Monthly Archives: November 2014

Aortic Stenosis

Aortic stenosis refers to narrowing of the aortic valve opening.  The three causes of aortic stenosis are 1) congenital abnormality resulting in one or two cusps of the valve rather than the normal variation of three, 2) calcification of the valve with increasing age and 3) rheumatic heart disease. Worldwide, the most common cause is rheumatic heart disease whereas in the United States, the most common cause is calcified disease and congenital bicuspid valve.

Signs, symptoms and complications

The clinical signs and symptoms of aortic stenosis vary depending on the time of presentation. When aortic stenosis is severe and progressed, the patients will develop heart failure, syncope or transient loss of consciousness and angina or pain caused by reduced blood flow to the heart due to obstruction of the coronary arteries. The most common symptoms include difficulty breathing, dizziness and angina with exertion. It is important to rule out non-cardiac causes of such symptoms including lung and gastrointestinal diseases.

On physical exam, patients with aortic stenosis will have a murmur described as systolic ejection murmur which is heard best in the right chest between ribs 2 and 3 and radiates to the carotid arteries. The intensity and timing of the murmur may be associated with the severity of the stenosis, with loud and late murmurs usually indicative of severe stenosis.

Aortic stenosis poses certain risks in patients which can have life threatening consequences. Patients with aortic stenosis can develop abnormal heart rhythms including atrial fibrillation, ventricular tachycardias and bradycardia or decreased heart rate. Abnormal heart rhythms can potentially cause sudden cardiac death. Patients are also at risk of developing ineffective endocarditis or an infection of the valve.  Other risks included increased tendency to bleed in the gastrointestinal tract, submucosal layer and skin and embolism or formation of blood clots in major blood vessels within the brain and body.

Diagnostic tests

The testing involved in evaluating a patient with aortic stenosis includes performing an electrocardiogram or EKG to check the rhythm of the heart, a chest X-ray to evaluate changes in the shape of the heart and valve calcifications and an echocardiogram (ECHO) which uses an ultrasound probe to evaluate the heart shape, valvular motion and pulmonary artery pressure. If the ECHO does not properly show the heart, a CT or MRI of the aorta may be necessary. In some cases, a cardiac catheterization may be warranted to measure the flow of blood through the valve.


Patients with aortic valve stenosis may be advised not to play strenuous sports, even if they do not have symptoms. Medications can be utilized to manage the symptoms associated with aortic stenosis, however they do not prevent the progression of valvular disease. Medications that treat heart failure, such as diuretics, beta blockers or nitrates may be used. High blood pressure due to aortic stenosis may also be treated with antihypertensives. However, this must be done slowly so the blood pressure does not drop suddenly.

Prophylactic antibiotics are currently not recommended for the prevention of infective endocarditis in patients who undergo dental procedures and subsequently develop bacteremia or blood infection.

The survival of patients with aortic stenosis dramatically decreases once patients develop signs of severe aortic stenosis including angina, syncope or heart failure.  Aortic valve replacement is recommended for patients who develop symptoms related to aortic stenosis and is considered the most effective treatment in order to improve survival. The aortic valve can be replaced surgically or with the use of a trans-catheter. Trans-catheter aortic valve implantation repairs the aortic valve without removing the old, damaged valve. A full collapsible valve is delivered to the site through a catheter. The new valve pushes the leaflets of the old valve out of the way and takes over the regulation of the blood flow.

For patients who do not develop symptoms, the American College of Cardiology and American Heart Association recommend valve replacement in patients who have a reduced ejection fraction (<50%), measured on an echocardiogram. Other factors considered for valve replacement include the likelihood of aortic stenosis progression which depends on age, calcification and coronary artery disease. The severity of stenosis based on specific valve dimensions and an abnormal stress test, a test used to assess the heart for ischemia or reduced perfusion can also play a role in the decision.


Aortic stenosis is narrowing of the aortic valve opening due to congenital abnormalities, age related calcifications and rheumatic heart disease. Patients with aortic stenosis can have no symptoms, mild symptoms or severe symptoms. The diagnosis of aortic stenosis relies on patient presentation as well as various tests. Patients who develop signs of severe aortic stenosis and do not receive aortic valve replacement have a poor prognosis.  When considering management of aortic stenosis, it is important to compare the combined risk of  aortic valve procedures and risk associated with prosthetic valves with the risk of complications and death due to aortic stenosis.


Lester SJ and Abbas AE. Aortic Stenosis, Chapter 17 of Current Diagnosis and Treatment Cardiology, 4th edition. McGraw Hill. 2014.

Otto, CM. Clinical  features and evaluation of aortic stenosis in adults. Uptodate. Last updated August 4, 2014.

Myocardial Perfusion PET Stress Test Indications

A myocardial perfusion scan is a nuclear medicine procedure. A tiny amount of a radioactive substance is used to examine the tissue under study and evaluate the heart’s function and blood flow. The radioactive tracer is absorbed by the healthy heart muscle tissue. On the scan, the areas that absorb the radionuclide will show up differently than the area that does not absorb the radionuclide, demarcating the healthy tissue from the damaged tissue.

A stress myocardial perfusion scan assessed blood flow to the heart muscle when it is stressed by exercise or medication and determines what areas of the heart have reduced blood flow during exercise. There are two types of myocardial perfusion scans, one that is used in conjunction with exercise and one that is used in conjunction with a pharmacological stressor. The exercise myocardial perfusion scan is done on a treadmill. The intensity of the exercise is gradually increased. When the patient reaches the maximum exercise point, determined by the heart rate and age, the radionuclide is injected into the IV line.

A pharmacological scan may be used for patients who cannot exercise on the treadmill for various reasons. Adenosine induces direct coronary artery dilation by activating the A2A receptor. This results in a 3.5-4 fold increase in myocardial blood flow.

This procedure evaluates the perfusion through the coronary arteries to the heart muscle using a radioactive tracer. It can show areas of the heart that are not getting sufficient blood flow. It is useful in patients with chest discomfort as it can determine if the discomfort comes from lack of blood flow to the heart muscle caused by narrowed or blocked arteries.

Major indications for a myocardial perfusion test are:

  • Diagnosis of CAD and various cardiac abnormalities
  • Identifying the location and degree of CAD in patients
  • Prognosis of patients who are at a risk of having a myocardial infarction, coronary aneurysm or wall motion abnormalities
  • Assessment of viable myocardium following heart attacks to justify revascularization
  • Post intervention reevaluation of the heart


Torsades de points, translated as “twisting of the spikes”, is a polymorphic ventricular tachycardia that exhibits distinct characteristics on an EKG. There is an illusion of a twisting of the QRS complex around the isoelectric baseline/It is hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness and syncope. Although most episodes of torsades de pointes revert to normal sinus rhythm within a few seconds, some may persist and degenerate into ventricular fibrillation. This can lead to sudden death if prompt medical attention is not given. Torsades de pointes is associated with long QT syndrome. The QT segment is greater than 400 ms on an EKG. This predisposes the patient to an R-on-T phenomenon. The R wave occurs during the relative refractory period at the end of repolarization and can initiate torsades.

Long QT syndrome can be inherited as congenital mutation of ion channels such as Jervell and Lange-Nielsen syndrome or acquired mutations of drugs that block these cardiac ion currents. Drugs that elongate QT segments include antiarrhythmics, amiodarone, methadone, lithium, chloroquine, erythromycin, amphetamine, methylphenidate and phenothiazines. Fluroquinolones can cause torsades by blocking the voltage-gated potassium channels. Taking cytochrome P450 inhibitors like fluoxetine, cimetidine and grapefruit juice in conjunction with medications metabolized by the P450 pathway such as clarithromycin, levofloxacin and haloperidol may elongate the QT interval. Other causes include diarrhea, hypomagnesemia and hypokalemia.

Torsades de pointes is treated by withdrawing the offending agent, infusing magnesium sulfate to correct the magnesium imbalance, antiarrhythmic drugs and electrical therapy such as a temporary pacemaker. Synchronized cardioversion may not be effective due to the polymorphic nature of torsades de pointes and the patient may require an unsynchronized shock.


Kawasaki disease is an acute febrile vasculitis that occurs in early childhood. It is recognized worldwide, although the greatest number of cases is in Japan. The most notable symptom is prolonged fever with abrupt onset and greater irritability than would be expected given the degree of fever. Non specific symptoms, such as irritability, vomiting, cough, diarrhea, weakness, abdominal pain and joint pain precede the onset of fever for a few days.

The clinical course is divided into three stages – acute, subacute and convalescent. The acute phase begins with an abrupt onset of fever and lasts 7-14 days. The fever tends to peak to 102-104* F and is not responsive to antibiotics and antipyretics. Most of the classic manifestations of Kawasaki disease, such as anterior uveitis, nonexudative bilateral conjunctivitis, perianal erythema, strawberry tongue and lip fissures, myocarditis and pericarditis, and lymphadenopathy occur during this stage. The mucocutaneous changes and lymphadenopathy are most evident during this stage but erythema and edema of the hands and feet may develop later. The diagnosis of Kawasaki disease is made in this stage.

The subacute phase stage begins when the fever has come down and lasts until week 4-6. This stage is characterized by desquamation of the digits, thrombocytosis, and the most dangerous consequence of Kawasaki disease – the development of coronary artery aneurysms. The risk for sudden death is highest in the subacute phase.

The convalescent phase usually occurs within 3 months of presentation and is marked by complete resolution of clinical signs of the illness. Acute phase reactants and other lab abnormalities begin to return to baseline levels. However, cardiac abnormalities may still be present. While smaller coronary artery aneurysms tend to resolve on their own, larger aneurysms may expand and cause a myocardial infarction.

The diagnosis of Kawasaki disease is based on clinical findings. The diagnostic criteria according to the American Heart Association is fever lasting longer than 5 days and 4 of the following 5 clinical findings:

  • Reddening of plasma and soles followed by desquamation
  • Polymorphous rash
  • Strawberry tongue, erythema or fissuring of the lips
  • Nonexudative conjunctivitis
  • Nonpurulent cervical lymphadenopathy, usually unilateral

There is no specific laboratory test to diagnose Kawasaki disease but acute-phase reactants such as ESR, CRP and alpha-1 antitrypsin levels are almost universally elevated at first and return to baseline 6-10 weeks after the onset of the illness. Levels of antineutrophil cytoplasmic antibodies, antiendothelial cell antibodies, antinuclear antibody and rheumatoid factors are all within the reference range. Culture tests and rapid antigen tests are negative. These tests can help narrow the differential diagnosis.

The treatment goal of Kawasaki disease is to prevent coronary artery aneurysms and to relieve symptoms. Full doses of IVIG are administered and the patient is monitored closely. Although Aspirin is contraindicated in pediatric populations, it is recommended for Kawasaki disease. High dose aspirin is used in the beginning of treatment, followed by lower dose aspirin for its antiplatelet effects. Kawasaki disease that is resistant to IVIG may benefit from intravenous plus corticosteroid therapy or infliximab infusion.

Patients must be monitored within 1 week of hospital discharge and have a repeat echocardiograph 21-28 days after the onset of fever. If baseline echos and echos at 3-4 weeks do not show any evidence of coronary aneurysms, further testing is usually not indicated. Patients with coronary aneurysms should remain on aspirin until the abnormalities resolve.


Takotsubo cardiomyopathy is a temporary heart condition that occurs predominantly in women. Its tendency to occur after severe emotional stress has given it the nickname “broken-heart syndrome.” Takotsubo cardiomyopathy is a weakening of the left ventricle after severe emotional or physical stress. The left ventricle balloons atypically. During systole, the mid section and apex balloon out while the base contracts normally. The shape is similar to that of a Japanese vessel used to catch octopuses called a takotsubo, hence the name. The exact mechanism is unclear, but experts think that a sudden surge in stress hormones, such as adrenaline, stuns the heart and triggers changes in heart muscle cells or coronary blood vessels that prevent the left ventricle from contracting effectively. Older women may be more vulnerable because of reduced levels of estrogen after menopause. Average age of onset is between 58-75 years. Less than 3% of cases occur in patients under age 50. Takotsubo cardiomyopathy can cause acute heart failure, lethal ventricular arrhythmias, and ventricular rupture.

Takotsubo cardiomyopathy has the following signs and symptoms:

  • Chest pain and shortness of breath after severe stress (emotional or physical)
  • Electrocardiogram abnormalities that mimic those of a heart attack
  • No evidence of coronary artery obstruction
  • Movement abnormalities in the left ventricle
  • Ballooning of the left ventricle
  • Recovery within a month

It is almost indistinguishable from a myocardial infarction. An EKG may also show ST-segment elevation. Other tests may be used to rule out a heart attack. An angiogram may be done to see if there is evidence of blockage of the coronary arteries. Cardiac biomarkers may show a small but rapid rise. In a heart attack, the biomarkers take longer to rise but peak higher. An echocardiogram may show the atypical ballooning of the left ventricle.

Takotsubo cardiomyopathy is temporary and usually resolves within a month. Clinicians usually prescribe beta-blockers, ACE inhibitors, and diuretics. They may also give aspirin to patients who have athereosclerosis. Beta blockers may be used long term to prevent recurrence by reducing the effects of adrenaline and other stress hormones. It is also important to identify and alleviate the underlying physical or emotional stress.

Most of the abnormalities in systolic function clear up in 1-4 weeks and most patients recover fully within two months. Intra-aortic balloon pump, fluids, and negative ionotropes such as beta blockers and calcium channel blockers may be used for treatment. Death is rare, but heart failure occurs in about 20% of the patients. It is treated with diuretics. Treatment with ionotropes can worsen the condition since the disease is due to a high catecholamine state. Rare complications include arrhythmias, obstruction of blood flow from the left ventricle, and rupture of the ventricle wall.


There are various causes of chest pain, both cardiac and non cardiac.  The associated symptoms are useful in determining the possible etiology of the pain and doing the appropriate test to diagnose it.

Anginal pain is substernal, brought on by exertion and is relieved by rest or nitroglycerin. It is brief, typically lasting 5-15 minutes. If the patient has a myocardial infarction, the pain is likely to be accompanied by diaphoresis. The pain may radiate to both arms and the patient may have low blood pressure. Both require an EKG for diagnosis and a myocardial infarction is a medical emergency. If the patient has a ripping or tearing pain and pulse abnormalities, they may have aortic dissection.

Chest pain can also be caused by pericarditis, which may follow a viral illness. Chest pain in pericarditis radiates to the back, neck or shoulders and often worsens when the patient inhales. It is improves by leaning forward.

Non cardiac causes of chest pain include pulmonary embolism, pneumothorax and pneumonia. Pulmonary embolism causes a sudden onset of pleuritic chest pain. Associated symptoms are fatigue, dyspnea, fainting, spitting up blood and cardiac arrest. Pneumothorax can cause pleuritic, sharp pain, usually accompanied by shortness of breath. Pneumonia pain is usually accompanied by fever, cough, altered breath sounds, wheezing and rales.

Non emergency chest pain can be caused by gastrointestinal condition such as reflux, esophageal spasm or peptic ulcer. In the case of reflux, the patient may feel food moving upward from the stomach.  The discomfort is worse after eating and when reclining. Chest wall pain is sharp, localized and worsens with movement. Patients may have a history of rheumatoid arthritis or osteoarthritis. The pain is also reproducible on palpation.

Chest pain can also be induced by drugs such as cocaine. However, patients are not likely to reveal a history of illicit drug abuse and may need to be tested.


Hypertrophic cardiomyopathy (HCM) is a genetic disease in which the heart muscle, or the myocardium, becomes abnormally thick. It is inherited in an autosomal dominant fashion and has variable penetrance. There are defects in the genes encoding for sarcomeric proteins, chiefly myosin heavy chain proteins. The hypertrophy is asymmetrical and occurs in the absence of an inciting stimulus. This thickened heart muscle can make it harder for the heart to pump blood efficiently. There is an abnormal arrangement of heart muscle cells, known as myofibril disarray, which can contribute to arrhythmia in some people/

Although most people with HCM are asymptomatic, symptoms can include dyspnea, syncope, angina, palpitations, dizziness and most devastatingly, sudden cardiac death. Although rare, sudden cardiac death has the highest incidence in adolescent and preadolescent children and is related to physical exertion. Physical findings may include double apical impulse, split second heart sound, systolic ejection crescendo-decrescendo murmur, jugular venous pulse revealing a prominent a wave. Complications include arrhythmias, obstructed blood flow, dilated cardiomyopathy, mitral valve problems, and heart failure.

Echocardiography is diagnostic for HCM. Findings may be summarized as:

  • Abnormal systolic anterior leaflet motion of mitral valve
  • Left ventricular hypertrophy
  • Left atrial enlargment
  • Small ventricular chamber size
  • Septal hypertrophy with septal to free wall ratio > 1.4:1
  • Mitral valve prolapse and mitral regurgitation
  • Decreased midaortic flow
  • Partial systolic closure of the aortic valve in midsystole

Since HCM presents variably, management depends on the presentation. Medications may include beta blockers, calcium channel blockers and rarely, diltiazem, amiodarone and disopyramide. Surgical treatments include left ventricular myomectomy, mitral valve replacement, permanent pacemaker implantation, catheter septal ablation and placement of an implantable cardioverter defibrillator.

Patient should avoid highly strenuous competitive athletic activity or physical exertion. No special diet is required. However, patients should maintain a healthy weight and avoid alcohol. Patients should avoid ionotropic drugs, nitrates, sympathomimetic amines and digitalis. Diuretics should be used with caution.


The pericardium is composed of two layers, an outer fibrous layer and an inner serous layer. Constrictive pericarditis is a chronic condition characterized by thickening of the outer fibrous layer. This forms a hard shell around the heart which limits diastolic filling, or the heart’s ability to expand when blood enters it. The main causes of constrictive pericarditis are due to processes that cause inflammation to develop around the heart. Such processes include heart surgery, radiation and tuberculosis, in regions where it is common.

Symptoms of constrictive pericarditis include dyspnea, fatigue, edema, ascites and weakness. On physical exam, elevated jugular venous pressure is present in almost all patients. The jugular venous pulse has a pronounced X descent.

Restrictive pericarditis involves the inner serous layer in addition to the outer fibrous layer. Patients present similarly to those with constrictive pericarditis, with dyspnea, edema, and ascites. However, the jugular venous pulse shows a steep Y descent.

Constrictive pericarditis can be differentiated from restrictive pericarditis based on the following diagnostic criteria:

Constrictive pericarditis Restrictive pericarditis
Short IVRT (isovolumic relaxation time) _ +
Sensitivity to respiration +
Short E wave deceleration time +
E/A ratio >1.0 +/- +
Peak pressure <50 mmHg +
RV ED/peak pressure >0.33 +

Definitive care for both constrictive and restrictive pericarditis is primarily surgical (ie, pericardiectomy). Operative therapy typically leads to rapid hemodynamic and symptomatic improvements. Patients with restrictive pericarditis may have a poorer response to pericardectomy than those with constrictive pericarditis because of the involvement of the serous layer.

Zetia proven to provide cardiovascular benefit according to a new study released by Merck &Co.

Merck&Co released a new study on November 17, 2014 providing new evidence that the drug Zetia, generic name ezetimibe, reduces major cardiovascular events when used as an adjunct to statin therapy.  The new study, referred to as IMPROVE-IT, showed a 6.4% reduction in cardiovascular events when combined with simvastatin 40mg.

Zetia works to block the uptake of cholesterol from the gastrointestinal tract, whereas statin therapies prevent cholesterol production in the liver.  The true advantage of taking Zetia has been debated.  A small study released in 2008, showed that while Zetia decreased cholesterol uptake, it did not reduce the amount of plaque build-up in the carotid arteries.  As a result, Zetia showed no clinical benefit for its use and many providers stopped prescribing it.

The new trial will change the perception of Zetia’s impact.  The trial, referred to as IMPROVE-IT, followed 18,144 high-risk patients over an average of 6 years.  The patients all had a history of a heart attack, unstable angina, arrhythmias or other ischemic symptoms with an LDL cholesterol level ≤ 125 mg/dL.  The initial goal was to prove that Zetia, when used in conjunction with a statin could lower LDL cholesterol, The study showed an average LDL reduction of 23% to 24% compared to patients on a statin alone.  The IMPROVE-IT trial actually went beyond its initial goal and showed a direct correlation between low levels of LDL and cardiovascular health.  Using Zetia as a dual agent suggested that 2 out of every 100 patients treated had a significant reduction in stroke or heart attack.

The impact of the trial will change many providers approach to cholesterol therapy.  Zetia is a different type of cholesterol lowering agent and the trial provided more insight into the effects of cholesterol, LDL and their effects on the body.

Long-Term Dual Anti-platelet Therapy After Stent Placement

What is it?

Aspirin 75-100 mg

+ P2Y12 receptor blocker (clopidogrel 75 mg daily; or prasugrel 10 mg daily, unless < 60 kg → 5 mg daily; or ticagrelor 90 mg twice daily).

Purpose: reduce the risk of stent thrombosis, which can lead to heart attack or death.

How long do you need to take it?

The optimal amount of time for antiplatelet therapy is unknown. However, 12 months is the standard duration for stable patients. After 12 months, only aspirin is continued for an indefinite period of time.

What is the minimum amount of time I should take antiplatelets?

4 weeks for bare metal stents

6 months for drug-eluting stents


Cutlip, D. (2014, August 4). Antiplatelet therapy after coronary artery stenting. UpToDate. Retrieved from

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