Category Archive Health A – Z

Atypical Bacterial Pneumonia /The word “pneumonia” takes its origin from the ancient Greek word “pneumon,” which means “lung,” so the word “pneumonia” becomes “lung disease.” Medically it is an inflammation of one or both lungs’ parenchyma that is more often, but not always, caused by infections. The many causes of pneumonia include bacteria, viruses, fungi, and parasites. This article will focus on bacterial pneumonia, as it is the major cause of morbidity and mortality. According to the new classification of pneumonia, there are four categories: community-acquired (CAP), hospital-acquired (HAP), healthcare-associated (HCAP) and ventilator-associated pneumonia (VAP). [rx][rx][rx]

Pneumonia is a lower respiratory tract infection, specifically involving the pulmonary parenchyma. Viruses, fungi, and bacteria can cause pneumonia. The severity of pneumonia can range from mild to life-threatening, with uncomplicated disease resolving with outpatient antibiotics and complicated cases progressing to septic shock, acute respiratory distress syndrome (ARDS) and death.[rx] It affects all age groups, accounts for over 2 million emergency visits annually, and is a leading cause of mortality in both adults and children. Atypical micro-organisms are known to cause a disproportionate disease burden in children and adolescents. Atypical organisms are difficult to culture.  They present subacutely and with progressive constitutional symptoms.[rx]

Types of Bacterial Pneumonia

• CAP: The acute infection of lung tissue in a patient who has acquired it from the community or within 48 hours of the hospital admission.
• HAP: The acute infection of lung tissue in a non-intubated patient that develops after 48 hours of hospitalization.
• VAP: A type of nosocomial infection of lung tissue that usually develops 48 hours or longer after intubation for mechanical ventilation.
• HCAP: The acute infection of lung tissue acquired from healthcare facilities such as nursing homes, dialysis centers, and outpatient clinics or from a patient with a history of hospitalization within the past three months.

Some articles include both HAP and VAP under the category of HCAP, so defining HCAP is problematic and controversial.

Causes of

Community-acquired pneumonia can be caused by an extensive list of agents that include bacteria, viruses, fungi, and parasites, but this article will focus on bacterial pneumonia and its causes. Bacteria have classically been categorized into two divisions on the basis of etiology, “typical” and “atypical” organisms. Typical organisms can be cultured on standard media or seen on Gram stain, but atypical organisms do not have such properties. [rx]

• Typical pneumonia refers to pneumonia caused by Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Group A streptococci, Moraxella catarrhalis, anaerobes, and aerobic gram-negative bacteria.
• Atypical pneumonia is mostly caused by Legionella, Mycoplasma pneumoniae, Chlamydia pneumoniae, and Chlamydia psittaci.
• Congestion – In this stage, pulmonary parenchyma is not fully consolidated, and microscopically, the alveoli have serous exudates, pathogens, few neutrophils, and macrophages.
• Red hepatization – In this stage, the lobe becomes consolidated, firm, and liver-like. Microscopically, there is an addition of fibrin along with serous exudate, pathogens, neutrophils, and macrophages. The capillaries are congested, and the alveolar walls are thickened.
• Gray hepatization – The lobe is still liver-like inconsistency but gray in color due to suppurative and exudate-filled alveoli.
• Resolution – After a week, it starts resolving as lymphatic drainage or a productive cough clears the exudate.

While taking the history, it is crucial to explore the patient’s potential exposures, risks of aspiration, host factors, and presenting symptoms.

Exposure – A detailed history of possible exposures should be sought as it can help in establishing the potential etiologies. The following are some associations of exposures and etiologies of bacterial pneumonia:

• Contaminated air-conditioning and water systems may cause legionella pneumonia
• Crowded places, such as jails, shelters, etc. expose a person to streptococcus pneumonia, mycobacteria, mycoplasma, and chlamydia
• Exposures to several animals, such as cats sheep, and cattle may lead to infection with Coxiella burnetii
• Some birds, such as chickens, turkeys, and ducks, can expose a person to Chlamydia psittaci.

Risks of Aspiration – Patients who have an increased risk of aspiration are more prone to develop pneumonia secondary to aspiration. Associated risks are:

• Altered mentation
• Drug abuse
• Dysphagia
• Gastroesophageal reflux disease (GERD)
• Alcoholism
• Seizure disorder

Host mechanisms – It is of utmost importance to explore a detailed history to find clues towards the etiology of pneumonia. For instance, a history of asthma, COPD, smoking, and immunocompromised status can be indicative of H influenza infection. H influenza most commonly appears in the winter season. Similarly, social, sexual, medication and family history can all be useful in determining the cause of illness.

Features in the history of bacterial pneumonia may vary from indolent to fulminant. Clinical manifestation includes both constitutional findings and findings due to damage to the lung and related tissue. The following are significant history findings:

• Fever with tachycardia and/or chills and sweats.
• The cough may be either nonproductive or productive with mucoid, purulent or blood-tinged sputum.
• Pleuritic chest pain if the pleura is involved.
• Shortness of breath with normal daily routine work.
• Other symptoms include fatigue, headache, myalgia, and arthralgia.

For unbeknownst reasons, the presence of rigors is more often indicative of pneumococcal pneumonia than other bacterial pathogens. [12]

The presence of productive cough is the most common and significant presenting symptom. Some bacterial causes have particular manifestation, such as:

• S pneumoniae – Rust-colored sputum
• Pseudomonas, Hemophilus – Green sputum
• Klebsiella – Red currant-jelly sputum
• Anaerobes – foul-smelling and bad-tasting sputum

Atypical pneumonia presents with pulmonary and extra-pulmonary manifestations, such as Legionella pneumonia, often presents with altered mentation and gastrointestinal symptoms.

Physical findings also vary from patient to patient and mainly depend on the severity of lung consolidation, the type of organism, the extent of the infection, host factors, and existence or nonexistence of pleural effusion. The following are major clinical findings:

• Increased temperature (usually more than 38 C or 100.4 F)[13]
• Decreased temperature (less than 35 C or 95 F)
• Increased respiratory rate (more than 18 breaths/min)
• Increased heart rate (more than 100/min)
• Bradycardia (less than 60/min)
• Cyanosis
• Percussion sounds vary from flat to dull
• Tactile fremitus
• Crackles, rales, and bronchial breath sounds are heard on auscultation
• Tracheal deviation
• Lymphadenopathy
• Pleural rub
• Egophony

Confusion manifests earlier in older patients. A critically ill patient may present with sepsis or multi-organ failure.

Some examination findings are specific for certain etiologies, such as:

• Bradycardia – Legionella
• Dental illnesses – Anaerobes
• Impaired gag reflex – Aspiration pneumonia
• Cutaneous nodules – Nocardiosis
• Bullous myringitis – Mycoplasma.

The approach to evaluate and diagnose pneumonia depends on the clinical status, laboratory parameters, and radiological evaluation.[14]

• Clinical Evaluation – It includes taking a careful patient history and performing a thorough physical examination to judge the clinical signs and symptoms mentioned above.
• Laboratory Evaluation – This includes lab values such as complete blood count with differentials, inflammatory biomarkers like ESR and C-reactive protein, blood cultures, sputum analysis or Gram staining and/or urine antigen testing or polymerase chain reaction for nucleic acid detection of certain bacteria.
• An arterial blood gas may reveal hypoxia and respiratory acidosis.
• Pulse oximetry of less than 92% indicates severe hypoxia and elevated CRP predicts a serious infection.[15]
• Blood cultures should be obtained before administering antibiotics. Unfortunately, they are only positive in 40% of cases.
• Sputum evaluation if good quality may reveal more than 25 WBC per low-power field and less than 10 squamous epithelial cells.
• Some bacterial causes present with specific biochemical evidence, such as Legionella may present with hyponatremia and microhematuria.
• Radiological Evaluation – It includes a chest x-ray as an initial imaging test and the finding of pulmonary infiltrates on plain film is considered as a gold standard for diagnosis when the lab and clinical features are supportive.[16][2]
• The chest x-ray may reveal a consolidation or parapneumonic effusion.
• Chest CT is done for complex cases where the cause is not known.
• Bronchoalveolar lavage is done in patients who are intubated and can provide samples for culture.

Treatment

In all patients with bacterial pneumonia, empirical therapy should be started as soon as possible. The first step in treatment is a risk assessment to know whether the patient should be treated in an outpatient or inpatient setting. Cardiopulmonary conditions, age, and severity of symptoms affect risk for bacterial pneumonia, especially CAP.[17][18][19]

An expanded CURB-65 or CURB-65 pneumonia severity score can be used for risk quantification. It includes C = Confusion, U = Uremia (BUN greater than 20 mg/dL), R = Respiratory rate (greater than 30 per min), B = B.P (BP less than 90/60 mmHg) and age greater than 65 years. One point is scored for each of these risk factors. For a score of 0-1, outpatient treatment is advised. If the total score is 2 or more, it indicates medical ward admission. If the total score is 3 or more, it indicates ICU admission. Recommended therapy for different settings are as follows:

• Outpatient Setting – For patients having comorbid conditions ( e.g., diabetes, malignancy, etc.), the regimen is fluoroquinolone or beta-lactams + macrolide. For patients with no comorbid conditions, macrolide or doxycycline can be used empirically. Testing is usually not performed as the empiric regimen is almost always successful.
• Inpatient Setting (non-ICU) – Recommended therapy is fluoroquinolone or macrolide + beta-lactam.
• Inpatient Setting (ICU) – Recommended therapy is beta-lactam + macrolide or beta-lactam + fluoroquinolone.
• MRSA: Vancomycin or linezolid can be added.

After getting a culture-positive lab result, therapy should be altered according to the culture-specific pathogen. The patient also can benefit from smoking cessation, counseling, and vaccination for influenza and pneumococcus. All patients treated at home should be scheduled for a follow-up visit within 2 days to assess any complication of pneumonia. The role of corticosteroids remains controversial and may be used in patients who remain hypotensive with presumed adrenal insufficiency.

Other measures

• Hydration
• Chest physical therapy
• Monitoring with pulse oximetry
• Upright positioning
• Respiratory therapy with bronchodilators
• Mechanical support if patients are in respiratory distress
• Nutrition
• Early mobilization

Complications

The most common complications of bacterial pneumonia are respiratory failure, sepsis, multiorgan failure, coagulopathy, and exacerbation of preexisting comorbidities. Other potential complications of bacterial pneumonia include:

• Lung fibrosis
• Destruction of lung parenchyma
• Necrotizing pneumonia
• Cavitation
• Empyema
• Pulmonary abscess
• Meningitis
• Death

References

Wallenberg syndrome is also known as lateral medullary syndrome or the posterior inferior cerebellar artery syndrome. Wallenberg described the first case in 1895. This neurological disorder is associated with a variety of symptoms that occur as a result of damage to the lateral segment of the medulla posterior to the inferior olivary nucleus. It is the most typical posterior circulation ischemic stroke syndrome in clinical practice. [rx][rx]

The vertebral arteries arise from the subclavian arteries. They enter the skull through the foremen magnum and merge to form the basilar artery at the pontomedullary junction. The posterior inferior cerebellar artery (PICA) is derived from each vertebral artery. PICA supplies the medulla and the suboccipital surface in the part of the cerebellum. When there is decreased blood flow to these regions, patients typically present with signs and symptoms of posterior circulation stroke which are discussed later.[rx]

Causes of Wallenberg Syndrome

Wallenberg syndrome is caused most commonly by atherothrombotic occlusion of the vertebral artery, followed most frequently by the posterior inferior cerebellar artery, and least often, the medullary arteries. Hypertension is the most prevalent risk factor, followed by smoking and diabetes. Cerebral embolism is a less frequent cause of the infarction. The other important cause to remember is vertebral artery dissection, which may have risk factors including neck manipulation or injury, Marfan syndrome, Ehlers Danlos syndrome, and fibromuscular dysplasia. Vertebral artery dissection is the commonest cause of Wallenberg syndrome in younger patients.[rx][rx]

Pathophysiology

The primary pathology of Wallenberg syndrome is occlusion of the posterior inferior cerebellar artery (PICA) or one of its branches[rx]. The syndrome can also be due to occlusion of the vertebral artery, or the inferior, middle, or superior medullary vessels. Anatomically the infarcted area in Wallenberg syndrome is supplied by the posterior inferior cerebellar artery (PICA). It turns out occlusion of the PICA accounts for only a small number of cases. The majority (80%) of cases are caused by occlusion of the vertebral artery, which gives rise to the PICA and the anterior spinal artery before it joins with the opposite vertebral artery to form the basilar artery. The most common mechanism of occlusion of the vertebral artery or PICA is atherothrombosis.[rx]

Atherosclerosis is the most common condition affecting the vertebrobasilar system, in which atheromatous plaques narrow and occlude large vessels. However, the pathology of small vessel disease is different as compared to that of large vessels which are affected by atherosclerosis. Small vessels are affected by a process called lipohyalinosis, which is closely associated with hypertension. Ischemic infarctions of these small vessels lead to small round infarctions called lacunae, which are scattered throughout the brainstem.[rx]

Diagnosis of Wallenberg Syndrome

A typical patient with Wallenberg syndrome is an elderly patient with vascular risk factors. Like any acute stroke syndrome, the onset is acute. The most common symptoms of onset are dizziness with vertigo, loss of balance with gait instability, hoarseness of voice, and difficulty swallowing. The symptoms often progress over several hours to sometimes a couple of days.

Usually, there is no weakness associated with this syndrome and so this condition is often misdiagnosed or missed. A careful neurological examination is a key to the diagnosis. A complete Wallenberg syndrome is not common, yet partial syndromes are satisfactory for the diagnosis most of the time. The important points in clinical diagnosis are a combination of crossed hemiparesis or hemianesthesia to indicate a brainstem lesion and the involvement of structures in the posterolateral medulla to localize, wherein the brainstem.

Different combinations of the following deficits may all be found in Wallenberg syndrome:

On the side of the lesion

• Vertigo with nystagmus (inferior vestibular nucleus and pathways). The nystagmus is typically central, beating to the direction of gaze. Nausea and vomiting, and sometimes hiccups, are associated with vertigo. Hiccups can often be intractable
• Dysphonia, dysarthria, and dysphagia (different nuclei and fibers of the IX and X nerves), often present with ipsilateral loss of gag reflex
• Horner syndrome; miosis, ptosis, and anhydrosis (sympathetic fibers)
• Ipsilateral ataxia with a tendency to fall to the ipsilateral side (inferior cerebellar hemisphere, spinocerebellar fibers, and inferior cerebellar peduncle)
• Pain and numbness with impaired facial sensation on the face (descending trigeminal tract)
• Impaired taste sensation (involvement of nucleus tractus solitarius)

On the contralateral side:

• Impaired pain and temperature sensation in the arms and legs (spinothalamic tract)
• It is important to note that there is no or only minimal weakness of the contralateral side (corticospinal fibers are ventral in location)

It is clinically interesting to note that more rostral lesions tend to be more ventrally located. These patients present with marked dysphagia and dysphonia due to the involvement of the nucleus ambiguus. More caudal lesions involve more dorsolateral structures. These patients present with vertigo, ataxia, nausea/vomiting, and Horner syndrome.[rx][rx][rx]

The clinical differential diagnoses include:

• Other causes of vertigo, especially peripheral vertigo such as acute labyrinthitis – the patient may be younger without any vascular risk factors. The nystagmus is peripheral and unidirectional or rotatory. There may be associated tinnitus without other brainstem signs. Head thrust test will be positive, which, if present, is most helpful in differentiating a central cause such as Wallenberg syndrome from a peripheral cause.[rx][rx]
• Hemorrhagic stroke – much less common, and headache is much more prominent.
• Acute demyelination in multiple sclerosis – patients are generally much younger, more likely female and known history of demyelinating disease
• Acute relapse/attack of neuromyelitis optica – with the involvement of the area postrema. The patient is most likely a young adult female, and the signs may suggest more than one central nervous system (CNS) lesion.

The diagnosis is usually made or suspected from a clinical exam and history of presentation. MRI with diffusion-weighted imaging (DWI) is the best diagnostic test to confirm the infarct in the inferior cerebellar area or lateral medulla.[rx] Up to 30% of patients with non-disabling stroke do not have a lesion on the DWI-MRI brain. These patients are DWI-negative stroke patients, and secondary prevention should be started to prevent future strokes. [rx]

A CT angiogram or MR angiogram is very helpful in identifying the site of vascular occlusion and to rule out uncommon causes such as vertebral artery dissection[rx].

An ECG is useful in excluding any underlying atrial fibrillation or unexpected acute coronary syndrome. Checking the serum electrolytes is essential. Patients with dysphagia or dysarthria need to be assessed by the speech pathologist before any food or medicine can be given orally.

Treatment of Wallenberg Syndrome

Similar to the management of any acute ischemic stroke, remember “TIME IS BRAIN.” Rapid evaluation is essential to an orderly approach (algorithm) developed within each hospital or stroke center. Management in certified stroke centers has shown to improve overall patient outcomes. Treatment aims at reducing the size of infarction and preventing any medical complication with the final target of improving patient outcome and prognosis.

The management steps include:

• Intravenous (IV) thrombolysis with IV – tissue plasminogen activator (TPA) within 3 to 4 1/2 hours of the onset of the ischemic stroke with slightly different exclusion criteria. Overall IV thrombolysis, within this time period, improves functional stroke outcomes by 30%. There have been studies showing that the window for posterior circulation strokes may be longer than 4 1/2 hours.[rx]
• Endovascular revascularization – the newer devices have been shown to improve outcome with the number needed to treat to be as low as 3. These are indicated mainly for large vessel intracranial occlusion which carries a very poor prognosis without revascularization.
• General medical therapy – patients are best monitored in the intensive care unit (ICU) for 24 hours after IV thrombolysis. Otherwise, it will be best to manage the patients in dedicated stroke beds or units.
• IV fluid – avoid hypotonic solution to reduce risks of cerebral edema. Normal saline is generally preferred.
• Blood pressure (BP)management – cerebral autoregulation is impaired in the infarcted areas of the brain. Blood pressure often comes down gradually without any drug treatment. In general, BP does not need to be lowered unless the patient receives IV thrombolysis or when it is over 220/120 mmHg.
• Speech therapy assessment – very important to prevent aspiration.
• Deep vein thrombosis prophylaxis – with sequential pressure devices and low dose heparin or low molecular weight heparin (LWMH).
• Blood sugar – best to keep the patient normoglycemic.
• Fever – the source of fever needs to be identified and treated. A simple antipyretic with acetaminophen is helpful.
• Antithrombotics – numerous more recent clinical trials failed to show any benefit or anticoagulants in acute stroke even in atrial fibrillation. Antithrombotic therapy with aspirin does improve the outcome.
• Early physical therapy and occupational therapy with a good plan for rehabilitation.

Secondary stroke prevention is decided after the outcome of the primary prevention of each patient. This will again include a multimodality approach:

• Carotid endarterectomy for significant large vessel extracranial stenosis
• Oral anticoagulation for cardioembolic strokes
• Antiplatelets such as aspirin, clopidogrel, or ASA/Dipyridamole for other forms of stroke
• Statins
• Smoking cessation
• Good control of diabetes
• Good blood pressure control
• Healthy diet and lifestyle with regular exercises

This multimodal approach can reduce the risk of subsequent stroke by 80%.[rx][rx][rx]

Physical Examination

• The presentation of myocardial infarction is variable. The patient may present fairly well-appearing or might be obviously in extremis. In every patient with chest pain, it is important to perform a focused physical exam.

 Obtain vital signs, including blood pressures in both arms.

For any patient presenting with chest pain concerning ACS, cardiac workup should be initiated, including history and exam as above, electrocardiogram (EKG), and cardiac biomarkers.

EKG

In a typical 12-lead EKG, posterior infarction is an indirect observation due to the placement of the leads. Limb leads placement is on each of the four extremities.

Precordial leads are placed on the anterior chest

• V1 – 4th intercostal space on the right margin of the sternum
• V2 – 4th intercostal space on the left margin of the sternum
• V4 – 5th intercostal space at the midclavicular line
• V3  – midway between V2 and V4
• V5 – 5th intercostal space on the anterior axillary line at the level of V4
• V6 – 5th intercostal space on the midaxillary line at the level of V4

Areas of infarction

• Inferior – II, III, aVF (RCA or LCx)
• Lateral – I, aVL, V5, V6 (LCx or diagonal branch of LAD)
• Septal – V1, V2 (LAD)
• Anterior – V2, V3, V4 (LAD)

ST-elevation is visible if there is inferior, lateral, or inferolateral involvement associated with a posterior extension. However, ST-elevation will not show on the typical EKG in isolated posterior MI, and other EKG changes may be observable. However, for further clarification, posterior leads (V7-V9) may be placed to evaluate further. [rx][rx][rx]

Posterior leads V7-V9 get placed on the posterior chest wall in the same horizontal plane as V6

• V7 – left posterior axillary line
• V8- the tip of the left scapula
• V9 – left paraspinal region

ST-elevation may be more subtle, and ST-elevation greater than 0.5 mm in one lead indicates posterior ischemia and is diagnostic for posterior ST-elevation MI (STEMI). When possible, compare to old EKGs.

Other changes that may present in posterior STEMI include

• ST-depression in the anterior leads, which may be deep (over 2 mm) and flat

• Large R-wave in V2-V3, which are larger than the S-wave

  • R-waves in V2-V3 that are greater than those in V4-V6 is an abnormal R-wave progression
• Large and upright anterior T waves
• Signs of ischemia in inferior and/or lateral territories, including possible ST elevation

• Mirror image effect of EKG regarding posterior wall ischemia

  • If turned upside down, tall anterior R-waves become deep posterior Q-waves, ST-depression becomes ST-elevation, and upright T-waves become inverted T-waves
  • If these changes are not present, it does not rule out posterior STEMI[rx][rx]

If there is an obvious posterior STEMI, and there is low suspicion of other pathology, the goal is to get the patient the lab for percutaneous intervention (PCI). There is no need to wait for lab results. IV access should be obtained, and labs sent. If there are more subtle EKG changes, but not definitive STEMI, consider serial EKGs. Sometimes on repeat EKGs, subtle ischemia evolves into STEMI.

ECG

The resting 12 lead ECG is the first-line diagnostic tool for the diagnosis of the acute coronary syndrome (ACS). It should be obtained within 10 minutes of the patient’s arrival in the emergency department.[rx] Acute MI is often associated with dynamic changes in the ECG waveform. Serial ECG monitoring can provide important clues to the diagnosis if the initial EKG is non-diagnostic at the initial presentation.[rx] Serial or continuous ECG recordings may help determine reperfusion or re-occlusion status. A large and prompt reduction in ST-segment elevation is usually seen in reperfusion.[rx]

ECG findings suggestive of ongoing coronary artery occlusion (in the absence of left ventricular hypertrophy and bundle branch block):[rx]

ST-segment elevation in two contiguous lead (measured at J-point) of

• Greater than 5 mm in men younger than 40 years, greater than 2 mm in men older than 40 years, or greater than 1.5 mm in women in leads V2-V3 and/or
• Greater than 1 mm in all other leads

ST-segment depression and T-wave changes

• New horizontal or down-sloping ST-segment depression greater than 5 mm in 2 contiguous leads and/or T inversion greater than 1 mm in two contiguous leads with prominent R waves or R/S ratio of greater than 1

The hyperacute T-wave amplitude, with prominent symmetrical T waves in two contiguous leads, maybe an early sign of acute MI that may precede the ST-segment elevation. Other ECG findings associated with myocardial ischemia include cardiac arrhythmias, intraventricular blocks, atrioventricular conduction delays, and loss of precordial R-wave amplitude (less specific finding).[14]

ECG findings alone are not sufficient to diagnose acute myocardial ischemia or acute MI as other conditions such as acute pericarditis, left ventricular hypertrophy (LVH), left bundle branch block (LBBB), Brugada syndrome, Takatsubo syndrome (TTS), and early repolarization patterns also present with ST deviation.

ECG changes associated with prior MI (in the absence of left ventricular hypertrophy and left bundle branch block)

• Any Q wave in lead V2-V3 greater than 0.02 s or QS complex in leads V2-V3
• Q wave > 03 s and greater than 1 mm deep or QS complex in leads I, II, aVL, aVF or V4-V6 in any two leads of contiguous lead grouping (I, aVL; V1-V6; II, III, aVF)
• R wave > 0.04 s in V1-V2 and R/S greater than 1 with a concordant positive T wave in the absence of conduction defect

Lab Studies

• CBC
• Metabolic profile
• Troponin
• Coagulation studies
• Consider  B-type natriuretic peptide (BNP) / NT pro-BNP

Imaging Studies

• Obtain bedside chest x-ray  – (CXR) or two-view CXR
• Consider bedside echocardiography – this is an operator-dependent skill but can be of significant value. Bedside echocardiography can evaluate for pericardial effusion, gross wall motion abnormalities, size of the ventricles, valvular abnormalities, and ejection fraction estimation. A suprasternal notch view is useful to visualize the aorta and evaluate for possible dissection. The proximal aorta is usually dilated with or without a visible intimal flap.
• Echocardiogram – Sound waves (ultrasound) create images of the moving heart. Your doctor can use this test to see how your heart’s chambers and valves are pumping blood through your heart. An echocardiogram can help identify whether an area of your heart has been damaged.
• Coronary catheterization (angiogram) – A liquid dye is injected into the arteries of your heart through a long, thin tube (catheter) that’s fed through an artery, usually in your leg or groin, to the arteries in your heart. The dye makes the arteries visible on X-ray, revealing areas of blockage.
• Cardiac CT or MRI – These tests create images of your heart and chest. Cardiac CT scans use X-rays. Cardiac MRI uses a magnetic field and radio waves to create images of your heart. For both tests, you lie on a table that slides inside a long tubelike machine. Each can be used to diagnose heart problems, including the extent of damage from heart attacks.
• Biomarker Detection of MI – Cardiac troponins (I and T) are components of the contractile apparatus of myocardial cells and expressed almost exclusively in the heart. Elevated serum levels of cardiac troponin are not specific to the underlying model of injury (ischemic vs. tension)[rx] [rx]. The rising and/or falling pattern of cardiac troponins (cTn) values with at least one value above the 99 percentile of upper reference limit (URL) associated with symptoms of myocardial ischemia would indicate an acute MI. Serial testing of cTn values at 0 hours, 3 hours, and 6 hours would give a better perspective on the severity and time course of the myocardial injury. Depending on the baseline cTn value, the rising/falling pattern is interpreted. If the cTn baseline value is markedly elevated, a minimum change of greater than 20% in follow up testing is significant for myocardial ischemia. Creatine kinase MB isoform can also be used in the diagnosis of MI, but it is less sensitive and specific than cTn level.[rx][rx]

Myocardial infarctions are generally clinically classified into ST-elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to an ECG.^[rx] STEMIs make up about 25 – 40% of myocardial infarctions.^[rx] A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:^[rx]

• Spontaneous MI related to plaque erosion and/or rupture fissuring, or dissection
• MI related to ischemia, such as from increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood pressure or low blood pressure
• Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a blood clot is found in a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood
• Associated with coronary angioplasty or stents
  • Associated with the percutaneous coronary intervention (PCI)
  • Associated with stent thrombosis as documented by angiography or at autopsy
• Associated with CABG
• Associated with spontaneous coronary artery dissection in young, fit women

Treatment of Acute ST-Elevation Myocardial Infarction (STEMI)

In summary,

• Early diagnosis – history, EKG, cardiac troponins
• Pain relief – nitroglycerin
• Hemodynamic stability – airway, breathing, circulation
• Reperfusion – PCI vs. fibrinolysis
• Prevention of thrombosis – aspirin plus P2Y12 inhibitor – clopidogrel vs. ticagrelor depending upon the choice of reperfusion
• Preventing life-threatening arrhythmias – beta-blocker therapy
• Improve prognosis and long term mortality – statins, aspirin, clopidogrel, beta-blockers, ACE inhibitors, revascularization, cardiac rehabilitation and aggressive lifestyle/behavioral modification

Reperfusion

• The definitive management of acute posterior STEMI is reperfusion therapy. Optimally this is done via percutaneous coronary intervention (PCI), though the next option would be fibrinolytic therapy. PCI is the preferred option if it can be initiated within 120 minutes, though within 90 minutes is the goal. If PCI is not available within 120 minutes, then fibrinolytic therapy should be given within 30 minutes.

Adjunctive Therapies

LifeStyle

• Smoking cessation – is the most cost-effective secondary measure to prevent MI. Smoking has a pro-thrombotic effect, which has a strong association with atherosclerosis and myocardial infarction.[rx]
• Diet, alcohol, and weight control – A diet low in saturated fat with a focus on whole grain products, vegetables, fruits, and the fish is considered cardioprotective. The target level for bodyweight is body mass index of 20 to 25 kg/m2  and waist circumference of <94 cm for the men and <80 cm for the female.[rx]

Complications

Complications of anteroseptal MI will include the complications of any myocardial infarction including:

• Myocardial dysfunction
• Heart failure
• Mechanical complication: Septal rupture, papillary muscle rupture, free wall rupture
• Septal rupture: Apical septum rupture is a rare complication but can occur with anteroseptal MI involving LAD lesion. Prompt diagnosis is necessary, and the treatment of choice is the definitive surgery.[rx]
• Papillary muscle rupture and free wall rupture are very uncommon with anteroseptal infarction. These complications are more related to multivessel disease.[rx]
• Conduction abnormalities – Conduction disturbances are associated with anteroseptal MI. One study showed that the right bundle branch block was the most common conduction abnormality in anteroseptal MI and it progressed to complete AV block in one-third of the patients.[rx]
• Post-infarction pericarditis

References

Risk factors for coronary artery disease classify into modifiable and non-modifiable risk factors.

A 2019 article indicated that age, sex, and race captured 63 to80% of prognostic performance, while modifiable risk factors contributed only modestly. Yet, control of modifiable risk factors led to substantial reductions in CAD events.[rx] Non-modifiable risk factors are discussed first:

• Age – CAD prevalence increases after 35 years of age in both men and women.  The lifetime risk of developing CAD in men and women after 40 years of age is 49% and 32%, respectively.[rx]
• Gender – Men are at increased risk compared to women.
• Ethnicity – African Americans, Hispanics, Latinos, and Southeast Asians, are ethnic groups with an increased risk of CAD morbidity and mortality.[rx][rx][rx]
• Family history – Family history is also a significant risk factor.  Patients with a family history of premature cardiac disease younger than 50 years of age have an increased CAD mortality risk.[rx] A separate article indicated that a father or brother diagnosed with CAD before 55 years of age, and a mother or sister diagnosed before 65 years of age are considered risk factors.[rx]

Modifiable risk factors have a smaller but still significant role.[rx] Yet, only two-thirds of patients receive optimal medication interventions.[rx] If this were achieved, there would be a substantial reduction in CAD events. One study observed that those with optimal risk factor profiles had a substantially lower rate of death from cardiovascular events.[rx]

Hypertension

In addition to these traditional cardiovascular risk factors, novel risk factors have also been subject to research.  These include:

Non-alcoholic fatty liver disease (NAFLD)

Testosterone

• In 2014, the FDA released a required labeling change for low testosterone products for the use of low testosterone due to aging, due to a possible increased risk of heart attack and stroke.  Subsequent studies and reviews have not been consistent in this correlation.  Some reviews have even indicated a potential beneficial cardiovascular effect when treating low testosterone with testosterone supplementation. Further study is needed to provide more clarity on this specific topic.[rx][rx][rx][rx][rx]

Vitamin D

Socioeconomic status

• Socioeconomic status is a significant risk factor for cardiovascular disease. Upstream determinants include financial strain, lack of affordable and nutritious food, exposure to domestic violence, and inadequate housing; this is an important consideration to consider given existing cardiovascular disease risk equations do not capture this.[rx]

Women and coronary artery disease (CAD)

• Although men are at higher risk than women of coronary artery disease, it is still the leading cause of death among women.  Among women, only 54% were aware of this in 2009. Cardiovascular disease caused approximately 1 in 3 female deaths.[rx] Women were found to have non-obstructive CAD in 57% of cases, in contrast to men who more commonly had obstructive CAD. Proposed mechanisms for this include coronary microvascular dysfunction (CMD), altered endothelial tone, structural changes, and altered response to vasodilator stimuli.[rx] Estrogen is thought to have a protective role in coronary vasoreactivity and is also theorized to promote plaque stabilization via an anti-inflammatory effect on atherosclerosis.[rx]
• Lack of awareness and understanding of coronary artery disease in women has also led to a disparity in health outcomes. There has been more focus on obstructive CAD and men compared to women.[rx][rx] One 2012 article reported a decrease in CAD mortality across all age groups in men and an increase in CAD mortality among young women (< 55 years old).[rx]

Symptoms of Coronary Artery Disease

Clinical Significance of Coronary Heart Disease

Hypertension

• The United States Preventive Services Task Force (USPSTF) gives a grade A recommendation for universal screening for hypertension in patients greater than 18 years of age and a grade I (current evidence insufficient) recommendation for screening for children and adolescents.[rx][rx]
• A systolic and diastolic blood pressure reduction of greater than 10mmHg and 5mmHg, respectively, led to a significant absolute risk reduction in CAD-related events (NNT 91).[rx]
• A systolic blood pressure reduction to a goal of 130mmHg reduced the incidence of CAD (NNT 27).[rx]
• A 2002 meta-analysis revealed that systolic blood pressure reduction of 20mmHg and diastolic blood pressure reduction of 10mmHg decreases the risk of death from coronary heart disease by about 50% between ages 40 to 49 and by about 1/3 between ages 80 to 89.[rx][rx][rx]

Hyperlipidemia

• The USPSTF recommends evaluation for statin use for the primary prevention of cardiovascular disease between 40 to 75 years of age.[rx] The USPSTF gives a grade I (current evidence insufficient) recommendation for routine screening for lipid disorders in children and adolescents.[rx]
• In 2011, the National Heart, Lung, and Blood Institute (NHLBI) recommended universal screening between 9 to 11 years of age and again at 17 to 21 years of age.  The American Academy of Pediatrics subsequently endorsed this.  Despite the publication of these guidelines, pediatric lipid screening practice patterns have not followed suit.[rx]
• An early 1994 review showed that a 10% reduction in serum cholesterol leads to a 50%, 40%, 30%, and 20% drop in CAD risk at age 20, 50, 60, and 70, respectively.[rx]
• The Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) study demonstrated that statins reduce the risk of major cardiovascular events.[rx] Treatment with a moderate-intensity statin resulted in a CAD absolute risk reduction of 2.7% (NNT 37). Treatment with a high-intensity statin resulted in a 4.1% absolute risk reduction (NNT 24).[rx]

Diabetes

• The USPSTF recommends screening for abnormal glucose in patients aged 40 to 70 years old who are overweight or obese.  Early screening for diabetes can also be a consideration for patients in higher-risk groups. This risk pool includes patients with a family history of diabetes, history of gestational diabetes or polycystic ovarian syndrome, or members of specified racial/ethnic groups (African Americans, American Indians, Alaskan Natives, Asian Americans, Hispanics or Latinos, Native Hawaiians or Pacific Islanders).[rx]
• The American Diabetes Association states that three years is a reasonable screening interval.
• A 2019 meta-analysis of 12 cardiovascular outcomes trials indicated that a 0.5% reduction in A1C conferred a 20% hazard risk reduction (95% CI 4-33%) for major cardiovascular events.  This analysis included patients on peptidase-4 inhibitors, GLP-1 agonists, and SGLT-2 inhibitors.[rx]

Diet

• The DASH, Mediterranean, and vegetarian diets have the most evidence for cardiovascular disease prevention.[rx]
• The DASH diet can reduce systolic blood pressure up to 11.5 mmHg in adults with hypertension.[rx][rx] A 2013 meta-analysis and systematic review revealed a 21% coronary artery disease risk reduction (RR 0.79, 95% CI 0.71-0.88) with the DASH diet.[rx]
• A 2017 meta-analysis and systematic review revealed an 8% risk reduction (15 studies, RR 0.92, 95% CI 0.90-0.95) of coronary artery disease for every 200 grams per day of fruits and vegetables. This effect was observable at up to 800 grams per day.[rx]
• A 2016 meta-analysis and systematic review revealed a 29% risk reduction (29 studies, RR 0.71, 95% CI 0.63-0.80) of coronary artery disease for every 28 grams per day of nut consumption.[rx]
• A 2017 narrative review revealed a decreased risk of about 20 to 25% with the Mediterranean diet on cardiovascular disease. It was also showed positive effects on endothelin function, arterial stiffness, and cardiac function.[rx]
• The American Heart Association recommends the replacement of saturated fat with polyunsaturated and monounsaturated fats.[rx] A 5% exchange in saturated fat consumption with polyunsaturated fat is associated with a 10% lower CAD risk (RR 0.90, 95% CI 0.83-0.97).[rx][rx] As noted above, a 2018 review, however, challenged the strength of the traditional link between saturated fat and higher CAD risk, compared to other nutrients.[rx] In a separate review, the lack of a significant association between saturated fat and cardiovascular disease was due to studies replacing saturated fat with highly refined carbohydrates.  If saturated fats were replaced by polyunsaturated fat, then coronary heart disease is indeed reduced.[rx]
• While it is challenging to carry out research relating to diet practices and coronary artery disease, much research has taken place in the past.[rx] The AHA/ACC guidelines recommend a diet consisting mostly of vegetables, fruits, legumes, nuts, whole grains, and fish. Dietary intake of processed meats, refined carbohydrates, and sweetened beverages should be reduced, while avoiding trans fats altogether. Saturated fats should be replaced with polyunsaturated and monounsaturated fats.[rx]
• The USPSTF recommends offering or referring adults who are obese/overweight and have one additional cardiovascular risk factor intensive behavioral counseling to promote a healthful diet and physical activity (Grade B).  The USPSTF also recommends individualizing the decision to offer or refer patients without obesity or other cardiovascular risk factors for behavioral counseling.

Smoking

• The USPSTF recommends screening for tobacco use in all adults with each clinical encounter and to provide behavioral and pharmacologic smoking cessation interventions.[rx] The USPSTF also recommends educating children and adolescents about the risks of smoking to prevent the initiation of tobacco use.
• The American Heart Association recommends a combined behavioral and pharmacologic approach to maximize quit rates.[rx]
• The risk of coronary artery disease drops to a level of lifetime nonsmokers within four years of quitting, according to the FDA, and within ten years, according to the CDC.[rx][rx]
• Behavioral interventions include motivational interviewing (Ask, Advise, Assess, Assist, Arrange for follow-up).
• Pharmacologic interventions such as nicotine replacement therapy, varenicline (Chantix), and bupropion (Wellbutrin) reduce cravings and withdrawal symptoms.
• A 2014 Cochrane review revealed that nicotine replacement therapies, such as nicotine gum and the nicotine patch increased the chances of smoking cessation by 49% (55 trials, RR 1.49, 95% CI 1.40-1.60) and 64% (43 trials, RR 1.64, 95% CI 1.52-1.78), respectively. The nicotine oral tablets/lozenges (6 trials, RR 1.95, 95% CI 1.61-2.36), inhaler (4 trials, RR 1.90, 95% CI 1.36-2.67), and nasal sprays (4 trials, RR 2.02, 95% CI 1.49-2.73) approximately doubled the chances of success.  The combination of bupropion and nicotine replacement therapy increased the likelihood of success by 24% compared to bupropion alone (4 trials, RR 1.24, 95% CI 1.06-1.45).[rx]
• Varenicline doubled the chances of smoking cessation.[rx] There have been rare reports of neuropsychiatric adverse effects with varenicline.  The FDA removed this black box warning in 2016 after noting that the risk was lower than expected.
• A 2014 Cochrane review showed that bupropion increases the chances of smoking cessation by 62% (44 trials, N=13,728, RR 1.62, 95% CI 1.48-2.78).[rx][rx]
• A 2016 Cochrane review indicated that the combined use of behavioral support and pharmacotherapy had a higher chance of success.[rx]

Obesity

• A patient’s body mass index (BMI) should be measured at each clinical encounter. The USPSTF recommends that practitioners offer obese adults a referral to a multicomponent behavioral interventionist.[rx]
• There is a large amount of evidence showing that in obese or overweight patients, even just a modest 5% body weight loss can lead to clinically significant health benefits.[rx]

Exercise

• The USPSTF recommends patients who are overweight, obese, or have CAD risk factors to intensive behavioral counseling for interventions to promote physical activity for the prevention of CAD.[rx][rx][rx]
• According to the National Health Interview Survey, only 20.9% of adults met the 2008 federal physical activity guidelines for aerobic and strengthening activity.[rx]
• Approximately 150 minutes per week of moderate-intensity aerobic activity reduces the risk of cardiovascular disease.[rx] Moderate-intensity aerobic exercise is defined as 50 to 70 percent of the patient’s maximum heart rate (220 beats per minute minus the patient’s age).  Any amount of physical activity has shown to have benefits in reducing CAD risk.[rx][rx] The most active patients have an approximately 35 to 40 percent risk reduction for coronary artery disease.
• The AHA/ACC guidelines also recommend resistance strength training to be incorporated into regular physical activity, as this can help improve physical function and ability to exercise.[rx][rx]

Aspirin in primary prevention

• Aspirin has long played a role in atherosclerotic cardiovascular disease prevention.  Although still established for secondary prevention, its use in primary prevention has more recently come into question due to a less favorable risk-benefit ratio [rx].  Recent evidence suggested a more tailored approach to the use of aspirin [rx].
• The USPSTF recommends aspirin for patients age 50 to 59 years of age, with a 10-year atherosclerotic cardiovascular disease risk, and do not have bleeding risk factors. Aspirin may be considered for those 60 to 69 years of age but may have less overall benefit and higher bleeding risk.[rx]

References

Risk factors for coronary artery disease classify into modifiable and non-modifiable risk factors.

A 2019 article indicated that age, sex, and race captured 63 to80% of prognostic performance, while modifiable risk factors contributed only modestly. Yet, control of modifiable risk factors led to substantial reductions in CAD events.[rx] Non-modifiable risk factors are discussed first:

• Age – CAD prevalence increases after 35 years of age in both men and women.  The lifetime risk of developing CAD in men and women after 40 years of age is 49% and 32%, respectively.[rx]
• Gender – Men are at increased risk compared to women.
• Ethnicity – African Americans, Hispanics, Latinos, and Southeast Asians, are ethnic groups with an increased risk of CAD morbidity and mortality.[rx][rx][rx]
• Family history – Family history is also a significant risk factor.  Patients with a family history of premature cardiac disease younger than 50 years of age have an increased CAD mortality risk.[rx] A separate article indicated that a father or brother diagnosed with CAD before 55 years of age, and a mother or sister diagnosed before 65 years of age are considered risk factors.[rx]

Modifiable risk factors have a smaller but still significant role.[rx] Yet, only two-thirds of patients receive optimal medication interventions.[rx] If this were achieved, there would be a substantial reduction in CAD events. One study observed that those with optimal risk factor profiles had a substantially lower rate of death from cardiovascular events.[rx]

Hypertension

In addition to these traditional cardiovascular risk factors, novel risk factors have also been subject to research.  These include:

Non-alcoholic fatty liver disease (NAFLD)

Testosterone

• In 2014, the FDA released a required labeling change for low testosterone products for the use of low testosterone due to aging, due to a possible increased risk of heart attack and stroke.  Subsequent studies and reviews have not been consistent in this correlation.  Some reviews have even indicated a potential beneficial cardiovascular effect when treating low testosterone with testosterone supplementation. Further study is needed to provide more clarity on this specific topic.[rx][rx][rx][rx][rx]

Vitamin D

Socioeconomic status

• Socioeconomic status is a significant risk factor for cardiovascular disease. Upstream determinants include financial strain, lack of affordable and nutritious food, exposure to domestic violence, and inadequate housing; this is an important consideration to consider given existing cardiovascular disease risk equations do not capture this.[rx]

Women and coronary artery disease (CAD)

• Although men are at higher risk than women of coronary artery disease, it is still the leading cause of death among women.  Among women, only 54% were aware of this in 2009. Cardiovascular disease caused approximately 1 in 3 female deaths.[rx] Women were found to have non-obstructive CAD in 57% of cases, in contrast to men who more commonly had obstructive CAD. Proposed mechanisms for this include coronary microvascular dysfunction (CMD), altered endothelial tone, structural changes, and altered response to vasodilator stimuli.[rx] Estrogen is thought to have a protective role in coronary vasoreactivity and is also theorized to promote plaque stabilization via an anti-inflammatory effect on atherosclerosis.[rx]
• Lack of awareness and understanding of coronary artery disease in women has also led to a disparity in health outcomes. There has been more focus on obstructive CAD and men compared to women.[rx][rx] One 2012 article reported a decrease in CAD mortality across all age groups in men and an increase in CAD mortality among young women (< 55 years old).[rx]

Symptoms of Coronary Heart Disease

Clinical Significance of Coronary Heart Disease

Hypertension

• The United States Preventive Services Task Force (USPSTF) gives a grade A recommendation for universal screening for hypertension in patients greater than 18 years of age and a grade I (current evidence insufficient) recommendation for screening for children and adolescents.[rx][rx]
• A systolic and diastolic blood pressure reduction of greater than 10mmHg and 5mmHg, respectively, led to a significant absolute risk reduction in CAD-related events (NNT 91).[rx]
• A systolic blood pressure reduction to a goal of 130mmHg reduced the incidence of CAD (NNT 27).[rx]
• A 2002 meta-analysis revealed that systolic blood pressure reduction of 20mmHg and diastolic blood pressure reduction of 10mmHg decreases the risk of death from coronary heart disease by about 50% between ages 40 to 49 and by about 1/3 between ages 80 to 89.[rx][rx][rx]

Hyperlipidemia

• The USPSTF recommends evaluation for statin use for the primary prevention of cardiovascular disease between 40 to 75 years of age.[rx] The USPSTF gives a grade I (current evidence insufficient) recommendation for routine screening for lipid disorders in children and adolescents.[rx]
• In 2011, the National Heart, Lung, and Blood Institute (NHLBI) recommended universal screening between 9 to 11 years of age and again at 17 to 21 years of age.  The American Academy of Pediatrics subsequently endorsed this.  Despite the publication of these guidelines, pediatric lipid screening practice patterns have not followed suit.[rx]
• An early 1994 review showed that a 10% reduction in serum cholesterol leads to a 50%, 40%, 30%, and 20% drop in CAD risk at age 20, 50, 60, and 70, respectively.[rx]
• The Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) study demonstrated that statins reduce the risk of major cardiovascular events.[rx] Treatment with a moderate-intensity statin resulted in a CAD absolute risk reduction of 2.7% (NNT 37). Treatment with a high-intensity statin resulted in a 4.1% absolute risk reduction (NNT 24).[rx]

Diabetes

• The USPSTF recommends screening for abnormal glucose in patients aged 40 to 70 years old who are overweight or obese.  Early screening for diabetes can also be a consideration for patients in higher-risk groups. This risk pool includes patients with a family history of diabetes, history of gestational diabetes or polycystic ovarian syndrome, or members of specified racial/ethnic groups (African Americans, American Indians, Alaskan Natives, Asian Americans, Hispanics or Latinos, Native Hawaiians or Pacific Islanders).[rx]
• The American Diabetes Association states that three years is a reasonable screening interval.
• A 2019 meta-analysis of 12 cardiovascular outcomes trials indicated that a 0.5% reduction in A1C conferred a 20% hazard risk reduction (95% CI 4-33%) for major cardiovascular events.  This analysis included patients on peptidase-4 inhibitors, GLP-1 agonists, and SGLT-2 inhibitors.[rx]

Diet

• The DASH, Mediterranean, and vegetarian diets have the most evidence for cardiovascular disease prevention.[rx]
• The DASH diet can reduce systolic blood pressure up to 11.5 mmHg in adults with hypertension.[rx][rx] A 2013 meta-analysis and systematic review revealed a 21% coronary artery disease risk reduction (RR 0.79, 95% CI 0.71-0.88) with the DASH diet.[rx]
• A 2017 meta-analysis and systematic review revealed an 8% risk reduction (15 studies, RR 0.92, 95% CI 0.90-0.95) of coronary artery disease for every 200 grams per day of fruits and vegetables. This effect was observable at up to 800 grams per day.[rx]
• A 2016 meta-analysis and systematic review revealed a 29% risk reduction (29 studies, RR 0.71, 95% CI 0.63-0.80) of coronary artery disease for every 28 grams per day of nut consumption.[rx]
• A 2017 narrative review revealed a decreased risk of about 20 to 25% with the Mediterranean diet on cardiovascular disease. It was also showed positive effects on endothelin function, arterial stiffness, and cardiac function.[rx]
• The American Heart Association recommends the replacement of saturated fat with polyunsaturated and monounsaturated fats.[rx] A 5% exchange in saturated fat consumption with polyunsaturated fat is associated with a 10% lower CAD risk (RR 0.90, 95% CI 0.83-0.97).[rx][rx] As noted above, a 2018 review, however, challenged the strength of the traditional link between saturated fat and higher CAD risk, compared to other nutrients.[rx] In a separate review, the lack of a significant association between saturated fat and cardiovascular disease was due to studies replacing saturated fat with highly refined carbohydrates.  If saturated fats were replaced by polyunsaturated fat, then coronary heart disease is indeed reduced.[rx]
• While it is challenging to carry out research relating to diet practices and coronary artery disease, much research has taken place in the past.[rx] The AHA/ACC guidelines recommend a diet consisting mostly of vegetables, fruits, legumes, nuts, whole grains, and fish. Dietary intake of processed meats, refined carbohydrates, and sweetened beverages should be reduced, while avoiding trans fats altogether. Saturated fats should be replaced with polyunsaturated and monounsaturated fats.[rx]
• The USPSTF recommends offering or referring adults who are obese/overweight and have one additional cardiovascular risk factor intensive behavioral counseling to promote a healthful diet and physical activity (Grade B).  The USPSTF also recommends individualizing the decision to offer or refer patients without obesity or other cardiovascular risk factors for behavioral counseling.

Smoking

• The USPSTF recommends screening for tobacco use in all adults with each clinical encounter and to provide behavioral and pharmacologic smoking cessation interventions.[rx] The USPSTF also recommends educating children and adolescents about the risks of smoking to prevent the initiation of tobacco use.
• The American Heart Association recommends a combined behavioral and pharmacologic approach to maximize quit rates.[rx]
• The risk of coronary artery disease drops to a level of lifetime nonsmokers within four years of quitting, according to the FDA, and within ten years, according to the CDC.[rx][rx]
• Behavioral interventions include motivational interviewing (Ask, Advise, Assess, Assist, Arrange for follow-up).
• Pharmacologic interventions such as nicotine replacement therapy, varenicline (Chantix), and bupropion (Wellbutrin) reduce cravings and withdrawal symptoms.
• A 2014 Cochrane review revealed that nicotine replacement therapies, such as nicotine gum and the nicotine patch increased the chances of smoking cessation by 49% (55 trials, RR 1.49, 95% CI 1.40-1.60) and 64% (43 trials, RR 1.64, 95% CI 1.52-1.78), respectively. The nicotine oral tablets/lozenges (6 trials, RR 1.95, 95% CI 1.61-2.36), inhaler (4 trials, RR 1.90, 95% CI 1.36-2.67), and nasal sprays (4 trials, RR 2.02, 95% CI 1.49-2.73) approximately doubled the chances of success.  The combination of bupropion and nicotine replacement therapy increased the likelihood of success by 24% compared to bupropion alone (4 trials, RR 1.24, 95% CI 1.06-1.45).[rx]
• Varenicline doubled the chances of smoking cessation.[rx] There have been rare reports of neuropsychiatric adverse effects with varenicline.  The FDA removed this black box warning in 2016 after noting that the risk was lower than expected.
• A 2014 Cochrane review showed that bupropion increases the chances of smoking cessation by 62% (44 trials, N=13,728, RR 1.62, 95% CI 1.48-2.78).[rx][rx]
• A 2016 Cochrane review indicated that the combined use of behavioral support and pharmacotherapy had a higher chance of success.[rx]

Obesity

• A patient’s body mass index (BMI) should be measured at each clinical encounter. The USPSTF recommends that practitioners offer obese adults a referral to a multicomponent behavioral interventionist.[rx]
• There is a large amount of evidence showing that in obese or overweight patients, even just a modest 5% body weight loss can lead to clinically significant health benefits.[rx]

Exercise

• The USPSTF recommends patients who are overweight, obese, or have CAD risk factors to intensive behavioral counseling for interventions to promote physical activity for the prevention of CAD.[rx][rx][rx]
• According to the National Health Interview Survey, only 20.9% of adults met the 2008 federal physical activity guidelines for aerobic and strengthening activity.[rx]
• Approximately 150 minutes per week of moderate-intensity aerobic activity reduces the risk of cardiovascular disease.[rx] Moderate-intensity aerobic exercise is defined as 50 to 70 percent of the patient’s maximum heart rate (220 beats per minute minus the patient’s age).  Any amount of physical activity has shown to have benefits in reducing CAD risk.[rx][rx] The most active patients have an approximately 35 to 40 percent risk reduction for coronary artery disease.
• The AHA/ACC guidelines also recommend resistance strength training to be incorporated into regular physical activity, as this can help improve physical function and ability to exercise.[rx][rx]

Aspirin in primary prevention

• Aspirin has long played a role in atherosclerotic cardiovascular disease prevention.  Although still established for secondary prevention, its use in primary prevention has more recently come into question due to a less favorable risk-benefit ratio [rx].  Recent evidence suggested a more tailored approach to the use of aspirin [rx].
• The USPSTF recommends aspirin for patients age 50 to 59 years of age, with a 10-year atherosclerotic cardiovascular disease risk, and do not have bleeding risk factors. Aspirin may be considered for those 60 to 69 years of age but may have less overall benefit and higher bleeding risk.[rx]

References

• Supraventricular (examples: atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), PSVT in the setting of pre-existing accessory conduction pathways)
• Ventricular (often secondary to mechanical/structural heart disease or channelopathies, such as Brugada)
• PR interval disorders/accessory conduction pathways (WPW, LGL, Mahaim syndrome, Breijo syndrome).

Bradyarrhythmia

• Sinus node dysfunction
• Atrioventricular conduction block (typically second or third degree)
• Pacemaker malfunction

Inherited channelopathies

• QT interval disorders (Long or short QT)

  • Romano-Ward syndrome: Autosomal dominant congenital long QT syndrome
  • Jervell and Lange-Nielsen syndrome: autosomal recessive long QT syndrome associated with deafness

• Brugada syndrome

  • An autosomal dominant mutation in the SCN5A gene, which encodes for voltage-gated sodium channels found in the heart

• Catecholaminergic polymorphic ventricular tachycardia

  • Autosomal dominant mutation of hRyR2 gene, which encodes for ryanodine receptors
  • Autosomal recessive mutation of CASQ2 gene, which encodes for calsequestrin-2
  • Drug-Induced(bradycardias, tachycardias, QT interval prolongation, cardiotoxins, etc.).[rx]

• https://www.ncbi.nlm.nih.gov/books/NBK442006/
• https://www.ncbi.nlm.nih.gov/books/NBK224/
• https://www.ncbi.nlm.nih.gov/books/NBK537285/
• https://www.ncbi.nlm.nih.gov/books/NBK459383/
• https://www.ncbi.nlm.nih.gov/books/NBK325/
• https://www.ncbi.nlm.nih.gov/books/NBK374/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258989/
• https://en.wikipedia.org/wiki/Syncope_(medicine)
• https://www.aafp.org/afp/2011/0915/p640.html
• https://www.medicinenet.com/fainting/article.htm
• https://my.clevelandclinic.org/health/diseases/17536-syncope
• https://www.heart.org/en/health-topics/arrhythmia/symptoms-diagnosis–monitoring-of-arrhythmia/syncope-fainting
• https://www.mayoclinic.org/diseases-conditions/vasovagal-syncope/symptoms-causes/syc-20350527
• https://www.healthline.com/health/types-of-syncope#how-to-help-others
• https://www.hopkinsmedicine.org/health/conditions-and-diseases/syncope-fainting
• https://www.msdmanuals.com/professional/cardiovascular-disorders/symptoms-of-cardiovascular-disorders/syncope

Sinus Node Dysfunction (SND) refers to a wide range of abnormalities involving sinus node impulse generation and propagation, leading to the inability of the sinus node to generate heart rates that are appropriate for the physiological needs. Causes of SND can be classified as intrinsic (secondary to a pathological condition involving the sinus node proper) or extrinsic (caused by depression of sinus node function by external factors such as drugs or autonomic influences).

The sinoatrial node (SA) is the default pacemaker and therefore a crucial component of the heart’s conduction system. It is located subepicardial and is crescent in shape. In an average adult, a sinoatrial node is 13.5 millimeters in length and is innervated by the vagus and sympathetic nerves. The sinoatrial nodal artery supplies blood to the sinoatrial node, it branches off the right coronary artery in 60% of cases, whereas in 40% of cases it comes off the left circumflex coronary artery.[rx][rx] Sinus bradycardia is a cardiac rhythm with appropriate cardiac muscular depolarization initiating from the sinus node generating less than 60 beats per minute (bpm). The diagnosis of sinus bradycardia requires visualization of an electrocardiogram showing a normal sinus rhythm at a rate lower than 60 bpm. Where a normal sinus rhythm has the following criteria[rx][rx]:

• Regular rhythm, with a P wave before every QRS.
• The p wave is upright in leads 1 and 2, P wave is biphasic in V1.
• The maximum height of a P wave is less than or equal to 2.5 mm in leads 2 and 3.
• The rate of the rhythm is between 60 bpm and 100 bpm.

Causes of Sinus Node Dysfunction

Sinus bradycardia has many intrinsic and extrinsic etiologies[rx][rx][rx][rx][rx][rx].

Both could result from abnormal mechanisms, including fibrosis, atherosclerosis, and inflammatory/infiltrative processes.

• Sinus Node Fibrosis – Replacement of the sinus node tissue by fibrous tissue is the most common cause of sinus node dysfunction, the replacement can also include other parts of the conduction system, including the AV node.[rx]
• Medication – Prescription medications can depress the sinus node function, potentially resulting in sinus node dysfunction include beta-blocker, non-dihydropyridine calcium channel blockers, digoxin, antiarrhythmic medications, and acetylcholinesterase inhibitors.[rx][rx][rx][rx][rx]
• Infiltrative disease – The SA node tissue can be affected during the disease process of some of the infiltrative diseases such as amyloidosis, sarcoidosis, scleroderma, hemochromatosis, and pericarditis leading to sinus node dysfunction.
• Ischemia – The sinus node is perfused by the sinoatrial nodal artery, which arises from the right coronary artery in 60 % of the time and from the left circumflex artery in 40 % of the time. Narrowing of this artery can lead to impairment of the sinus node function leading to sinus node dysfunction that can be potentially reversible. Almost all such cases are present in inferior myocardial infarction.[rx][rx]
• Familial – Sinus node dysfunction in rare cases can be the result of cardiac sodium channel mutations of SCN5A and HCN4 genes.[rx]
• Miscellaneous – Other disorders that can rarely cause sinus node dysfunction to include hypothyroidism, hypothermia, and hypoxia.

Inherent Etiologies

• Chest trauma
• Ischemic heart disease
• Acute myocardial infarction
• Acute and chronic coronary artery disease
• Repair of congenital heart disease
• Sick sinus syndrome
• Radiation therapy
• Amyloidosis
• Pericarditis
• Lyme disease
• Rheumatic fever
• Collagen vascular disease
• Myocarditis
• Neuromuscular disorder
• X-linked muscular dystrophy
• Familial disorder
• Inherited channelopathy

Extrinsic Etiologies

• Vasovagal simulation (endotracheal suctioning)
• Carotid sinus hypersensitivity
• Beta-blockers
• Calcium channel blockers
• Digoxin
• Ivabradine
• Clonidine
• Reserpine
• Adenosine
• Cimetidine
• Antiarrhythmic Class I to IV
• Lithium
• Amitriptyline
• Narcotics
• Cannabinoids
• Hypothyroidism
• Sleep apnea
• Hypoxia
• Intracranial hypertension
• Hyperkalemia
• Anorexia nervosa

Diagnosis of Sinus Node Dysfunction

Laboratory studies that should be ordered include:

• Glucose level
• Electrolytes
• Calcium, magnesium
• Thyroid function
• Troponin
• Toxicological drug screen

A 12-lead ECG is necessary to make the diagnosis.

What Is Sinus Node Dysfunction?/Sinus Node Dysfunction (SND) refers to a wide range of abnormalities involving sinus node impulse generation and propagation, leading to the inability of the sinus node to generate heart rates that are appropriate for the physiological needs. Causes of SND can be classified as intrinsic (secondary to a pathological condition involving the sinus node proper) or extrinsic (caused by depression of sinus node function by external factors such as drugs or autonomic influences).

The sinoatrial node (SA) is the default pacemaker and therefore a crucial component of the heart’s conduction system. It is located subepicardial and is crescent in shape. In an average adult, a sinoatrial node is 13.5 millimeters in length and is innervated by the vagus and sympathetic nerves. The sinoatrial nodal artery supplies blood to the sinoatrial node, it branches off the right coronary artery in 60% of cases, whereas in 40% of cases it comes off the left circumflex coronary artery.[rx][rx] Sinus bradycardia is a cardiac rhythm with appropriate cardiac muscular depolarization initiating from the sinus node generating less than 60 beats per minute (bpm). The diagnosis of sinus bradycardia requires visualization of an electrocardiogram showing a normal sinus rhythm at a rate lower than 60 bpm. Where a normal sinus rhythm has the following criteria[rx][rx]:

• Regular rhythm, with a P wave before every QRS.
• The p wave is upright in leads 1 and 2, P wave is biphasic in V1.
• The maximum height of a P wave is less than or equal to 2.5 mm in leads 2 and 3.
• The rate of the rhythm is between 60 bpm and 100 bpm.

Causes of Sinus Node Dysfunction

Sinus bradycardia has many intrinsic and extrinsic etiologies[rx][rx][rx][rx][rx][rx].

Both could result from abnormal mechanisms, including fibrosis, atherosclerosis, and inflammatory/infiltrative processes.

• Sinus Node Fibrosis – Replacement of the sinus node tissue by fibrous tissue is the most common cause of sinus node dysfunction, the replacement can also include other parts of the conduction system, including the AV node.[rx]
• Medication – Prescription medications can depress the sinus node function, potentially resulting in sinus node dysfunction include beta-blocker, non-dihydropyridine calcium channel blockers, digoxin, antiarrhythmic medications, and acetylcholinesterase inhibitors.[rx][rx][rx][rx][rx]
• Infiltrative disease – The SA node tissue can be affected during the disease process of some of the infiltrative diseases such as amyloidosis, sarcoidosis, scleroderma, hemochromatosis, and pericarditis leading to sinus node dysfunction.
• Ischemia – The sinus node is perfused by the sinoatrial nodal artery, which arises from the right coronary artery in 60 % of the time and from the left circumflex artery in 40 % of the time. Narrowing of this artery can lead to impairment of the sinus node function leading to sinus node dysfunction that can be potentially reversible. Almost all such cases are present in inferior myocardial infarction.[rx][rx]
• Familial – Sinus node dysfunction in rare cases can be the result of cardiac sodium channel mutations of SCN5A and HCN4 genes.[rx]
• Miscellaneous – Other disorders that can rarely cause sinus node dysfunction to include hypothyroidism, hypothermia, and hypoxia.

Inherent Etiologies

• Chest trauma
• Ischemic heart disease
• Acute myocardial infarction
• Acute and chronic coronary artery disease
• Repair of congenital heart disease
• Sick sinus syndrome
• Radiation therapy
• Amyloidosis
• Pericarditis
• Lyme disease
• Rheumatic fever
• Collagen vascular disease
• Myocarditis
• Neuromuscular disorder
• X-linked muscular dystrophy
• Familial disorder
• Inherited channelopathy

Extrinsic Etiologies

• Vasovagal simulation (endotracheal suctioning)
• Carotid sinus hypersensitivity
• Beta-blockers
• Calcium channel blockers
• Digoxin
• Ivabradine
• Clonidine
• Reserpine
• Adenosine
• Cimetidine
• Antiarrhythmic Class I to IV
• Lithium
• Amitriptyline
• Narcotics
• Cannabinoids
• Hypothyroidism
• Sleep apnea
• Hypoxia
• Intracranial hypertension
• Hyperkalemia
• Anorexia nervosa

Diagnosis of Sinus Node Dysfunction

Laboratory studies that should be ordered include:

• Glucose level
• Electrolytes
• Calcium, magnesium
• Thyroid function
• Troponin
• Toxicological drug screen

A 12-lead ECG is necessary to make the diagnosis.

Diagnosis of Ischemic Cardiomyopathy

After getting a detailed history and physical examination, there are several diagnostic modalities which can help with the diagnosis of ischemic cardiomyopathy.

• Electrocardiogram (ECG) – important for identifying evidence of acute or prior myocardial infarction or acute ischemia, also rhythm abnormalities, such as atrial fibrillation.
• Blood test – Cardiac troponin (T or I), complete blood count, serum electrolytes, blood urea nitrogen, creatinine, liver function test and brain natriuretic peptide (BNP). BNP (or NT-proBNP) level adds greater diagnostic value to the history and physical examination than other initial tests mentioned above.
• Transthoracic Echocardiogram – to determine ventricular function and hemodynamics.
• Chest x-ray – Simple and readily available test. It may show cardiomegaly and other findings of heart failure if a patient has progressed to that stage. Some x-ray findings in heart failure patients include pulmonary congestion, Kerley B lines, pleural effusion, and blunting of costophrenic angle.
• ECG – Assesses the electrical activity of the heart. Useful in looking at the heart rate, rhythm, past/current ischemic episode, chamber enlargement, and information about heart’s electrical conductivity.
• Transthoracic echocardiography (TTE) –  This ultrasound-based imaging modality is useful in looking at cardiac anatomy and valvular function. It will assess for ventricular systolic/diastolic function, cardiac wall motion, pericardial pathology, and valvular function. All this information is useful in diagnosing ischemic cardiomyopathy.
• Cardiac stress test – There are different stress tests available depending on the patient’s health, functional status, baseline heart rhythm, and exercise tolerance. The goal of these stress tests is to assess for cardiac ischemia. Some stress test modality can also provide information about myocardial viability.
• Coronary angiography – allows for direct visualization of the coronary arteries, level of obstruction, and the blood flow to the myocardium. They also use it for percutaneous coronary intervention (PCI) with balloon angioplasty and coronary stents to allow for better blood flow across the occluded coronary artery.
• CTCA – It uses computed tomography (CT) to take angiograms of the coronary arteries. Aids with the diagnosis of CAD in patients with low-intermediate risk.
• Brain natriuretic peptide (BNP) test – BNP is synthesized in the ventricles, and it is secreted when the myocardial muscle has a high wall tension. Important biomarker for heart failure patients.
• Cardiac magnetic resonance imaging- Differentiate ischemic from non-ischemic cardiomyopathies using Late gadolinium imaging. Late Gadolinium Enhancement (LGE) reflects irreversible damage to the myocardium and fibrosis. When LGE is absent in a dysfunctional segment of the myocardium, it implies the potential for recovery with time (stunning) or by medical treatment or revascularization.

Treatment of Ischemic Cardiomyopathy

Ischemic cardiomyopathy is managed primarily with an optimal goal-directed medical therapy (GDMA). However, for appropriate patient population cardiac intervention for revascularization is a common treatment option. Foremost, the patient will benefit from lifestyle modification which includes smoking cessation, exercise, and diet changes. Below are the medical interventions that can be done to optimize patients with ICM.

• Revascularization – Patients with ischemic cardiomyopathy may benefit from revascularization. There was a 7% absolute reduction in overall mortality over a 10-year time between patients who had CABG versus GDMA[rx]. Revascularization followed by GDMA is recommended for these patients; however, it is important to assess their procedural candidacy. The primary goal is to reperfuse viable ischemic areas of the myocardium. However, a general test for myocardial viability is not recommended.
• Aspirin – It is shown to have major reductions in cardiovascular morbidity and mortality for patients with coronary heart disease. Historically, low dose aspirin (75 to 100 mg) once daily used; however, new data suggest that patients may need a higher dose (300 to 325 mg) if they weigh over 70 kg[rx].
• Beta-adrenergic antagonist (beta-blockers) – Atenolol, esmolol, labetalol, metoprolol, and propranolol. This group antagonizes the effects of epinephrine on beta receptors on the heart. B1 receptors are present in the heart, and when antagonized they decrease heart rate and heart muscle contractility that leads to decreasing oxygen consumption by the heart. B1 selective blockers decrease mortality in patients with heart failure, but should not be initiated when the patient is having acutely decompensated heart failure.
• High Potency Statin – Atorvastatin 40 to 80 mg or rosuvastatin 20 to 40 mg orally once daily. The mechanism of action is via HMG-CoA reductase inhibition. These medications inhibit the conversion of HMG-CoA to mevalonate, which is a cholesterol precursor. Statins decrease mortality in patients with coronary artery disease (CAD).
• Angiotensin-converting enzyme (ACE) inhibitors – Enalapril, lisinopril, captopril, and ramipril. This group of antihypertensive medications decreases mortality in patients with heart failure. The inhibition of the ACE leads to a decrease of angiotensin II which, when inhibited, decreases glomerular filtration rate by preventing constriction of efferent arterioles. This class of medication has cardio and renal protective effects when it comes to remodeling. An undesired added effect is the prevention of inactivation of bradykinin, which is a potent vasodilator that produces a cough and possibly angioedema in patients with C1 esterase inhibitor deficiency.
• Angiotensin II receptor blockers (ARB) – Valsartan, losartan, candesartan. This group has the same effect as the ACEI by selectively blocking angiotensin II from binding in its AT1 receptor. This group does not affect bradykinin and therefore is the medication of choice, replacing ACE inhibitors, when a patient complains of a cough or presents with angioedema after being started on ACEI.
• Hydralazine and nitrate – This group of medication can be used in patients who are unable to tolerate ACEI or an ARB.
• Angiotensin receptor neprilysin inhibitor (ARNI) – Recent clinical trial, PARADIGM-HF, showed a reduction in cardiovascular and all-cause mortality along with a reduction in heart failure hospitalization while on valsartan/sacubitril compared to enalapril[rx].
• Spironolactone – Shown to reduce morbidity and mortality in patients with heart failure (NYHA class III and IV) with LVEF 35% or less. It is a potassium-sparing diuretic that works as an antagonist to the aldosterone receptor at the nephron’s cortical collecting tubule.
• Digoxin – does not decrease mortality but is helpful in decreasing symptoms and hospitalizations in patients with congestive heart failure (CHF). Digoxin works by inhibiting the effects of the enzyme sodium/potassium ATPase in the heart muscle, stopping the sodium/calcium exchange, leaving more calcium inside the cell which increases contractility.
• ICD placement – Select patients with ischemic cardiomyopathy qualify for ICD to prevent sudden cardiac death (SCD). Patients with ischemic cardiomyopathy (evaluated at least 40 days post-MI or 3 months after revascularization), LVEF of 35% or less, and associated heart failure (HF) with New York Heart Association (NYHA) functional class II or III status, there is a class IA recommendation for ICD placement. Additionally, if a patient with ICM has LVEF of 30% or less and NYHA class I, ICD therapy is indicated for primary prevention of SCD.
• Biventricular pacing – If a patient has ischemic cardiomyopathy and LVEF 35% or less, then they may be a candidate for cardiac resynchronization therapy (CRT) if their heart failure symptoms are not controlled despite revascularization and GDMA.

Ultimately, a heart transplant is the only option when the disease progresses, and no alleviation is achieved with the intervention mentioned above.

Prevention

Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided. Currently practiced measures to prevent cardiovascular disease include:

• Reduction in consumption of saturated fat – there is moderate-quality evidence that reducing the proportion of saturated fat in the diet, and replacing it with unsaturated fats or carbohydrates over a period of at least two years, leads to a reduction in the risk of cardiovascular disease.^[rx]
• Stopping smoking and avoidance of second-hand smoke.^[rx] Stopping smoking reduces risk by about 35%.^[rx]
• Maintain a healthy diet, such as the Mediterranean diet. Dietary interventions are effective in reducing cardiovascular risk factors over a year, but the longer-term effects of such interventions and their impact on cardiovascular disease events are uncertain.^[rx]
• At least 150 minutes (2 hours and 30 minutes) of moderate exercise per week.
• Limit alcohol consumption to the recommended daily limits;^[rx] People who moderately consume alcoholic drinks have a 25–30% lower risk of cardiovascular disease. However, people who are genetically predisposed to consume less alcohol have lower rates of cardiovascular disease^[rx] suggesting that alcohol itself may not be protective. Excessive alcohol intake increases the risk of cardiovascular disease and consumption of alcohol is associated with increased risk of a cardiovascular event in the day following consumption.^[rx]
• Lower blood pressure, if elevated. A 10 mmHg reduction in blood pressure reduces risk by about 20%.^[rx]
• Decrease non-HDL cholesterol. Statin treatment reduces cardiovascular mortality by about 31%.^[rx]
• Decrease body fat if overweight or obese.^[rx] The effect of weight loss is often difficult to distinguish from dietary change, and evidence on weight reducing diets is limited.^[rx] In observational studies of people with severe obesity, weight loss following bariatric surgery is associated with a 46% reduction in cardiovascular risk.^[rx]
• Decrease psychosocial stress.^[rx] This measure may be complicated by imprecise definitions of what constitutes psychosocial interventions.^[rx] Mental stress-induced myocardial ischemia is associated with an increased risk of heart problems in those with previous heart disease.^[rx] Severe emotional and physical stress leads to a form of heart dysfunction known as Takotsubo syndrome in some people.^[rx] Stress, however, plays a relatively minor role in hypertension.^[rx] Specific relaxation therapies are of unclear benefit.

References