A 60-year-old male patient is receiving aspirin, an angiotensin-converting enzyme inhibitor, nitrates, and a beta-blocker for chronic stable angina. He presents to the ER with an episode of more severe and long-lasting anginal chest pain each day over the past 3 days. His ECG and cardiac enzymes are normal.
Which of the following is the best course of action?
This patient presents with acute coronary syndrome, a change from the previous chronic stable state in that his chest pain has become more frequent and more severe. Antithrombotic therapy with intravenous heparin is indicated, along with additional antiplatelet therapy using clopidogrel. Subcutaneous administration of low-molecular-weight heparin (such as enoxaparin) is an alternative. There is no role for digoxin, as this may increase myocardial oxygen consumption and exacerbate the situation. Thrombolytic therapy is reserved for the treatment for ST-segment elevation myocardial infarction, and does not reduce cardiac events in the setting of unstable angina. The patient is at high risk for myocardial necrosis and should be admitted to the hospital for stabilization, but simple observation and failure to intensify his treatment would be inappropriate. A more aggressive approach is early interventional cardiac catheterization with angioplasty and/or stent placement, possibly in conjunction with glycoprotein IIb/IIIa inhibitors.
You have been asked to evaluate a 42-year-old white male smoker who presented to the emergency department with sudden onset of crushing substernal chest pain, nausea, diaphoresis, and shortness of breath. His initial ECG revealed ST segment elevation in the anteroseptal leads. Cardiac enzymes were normal. The patient underwent emergent cardiac catheterization, which revealed only a 25% stenosis of the left anterior descending (LAD) artery. No percutaneous intervention was performed. Which of the following interventions would most likely reduce his risk of similar episodes in the future?
This patient’s presentation and minimal coronary artery disease are most consistent with Prinzmetal variant angina. Prinzmetal angina is caused by severe spasm of an epicardial coronary artery. The area of vasospasm is often near a nonhemodynamically significant atherosclerotic lesion. Patients tend to be smokers and are often younger than patients who present with atherosclerotic coronary artery disease. In this case, the patient’s mild LAD stenosis does not explain the degree of ischemia evidenced by the ST segment elevation. Percutaneous intervention has not been shown to be useful in management of Prinzmetal angina, as the culprit is transient vasospasm rather than fixed obstruction. Calcium-channel blockers are the mainstay of therapy to prevent recurrence of spasm. ACE inhibitors and beta-blockers do not prevent acute vasospasm. Of course, the patient should also be counseled to abstain from smoking.
A 15-year-old student presents to your office on the advice of his football coach. The patient started playing football this year and suffered a syncopal episode at practice yesterday. He reports that he was sprinting with the rest of the team and became light-headed. He lost consciousness and fell to the ground, regaining consciousness within 1 or 2 minutes. He has had no prior episodes of syncope. The patient is adopted and family history unavailable. Physical examination reveals a systolic murmur heard at the left lower sternal border and apex. ECG reveals sinus rhythm with evidence of left ventricular hypertrophy (LVH). What physical examination findings would likely be present?
The patient has hypertrophic cardiomyopathy, which is one of the causes of exertional syncope in young persons and is associated with left ventricular hypertrophy on EKG. The typical murmur of hypertrophic cardiomyopathy is a harsh systolic diamond-shaped murmur heard best at the lower sternal border and apex. Factors that increase myocardial contractility (eg, exercise, sympathomimetics, or aminophylline) and decrease preload (eg, Valsalva maneuver, standing or nitroglycerin) reduce left ventricular end-diastolic volume, increase the turbulence of blood flow exiting the ventricle during systole, and hence accentuates the murmur. On the other hand, elevation of arterial pressure (squatting and hand grip), increase in venous return or preload (leg raising), and expansion of blood volume (pregnancy) all increase left ventricular volume and decrease intensity of the murmur. Choice b is a typical murmur of mitral valve prolapse (MVP) which is characterized by a mid- or late- (nonejection) systolic click. The click may be followed by a highpitched, late-systolic crescendo-decrescendo murmur heard best at the apex. The click and murmur occur earlier with maneuvers that decrease left ventricular volume which exaggerates the propensity of mitral leaflet prolapse. These maneuvers include standing, and the Valsalva maneuver. Maneuvers that increase left ventricular volume, such as squatting and isometric exercise diminish the degree of prolapse, and the click-murmur is delayed and decreases in intensity. Choice c is a murmur of mitral regurgitation (MR). It is usually holosystolic, best heard at the apex, and radiates to the axilla. The systolic murmur of chronic MR not due to MVP is intensified by isometric exercise (handgrip) but is reduced with the Valsalva maneuver. Choice d is a murmur of tricuspid regurgitation. It is usually a blowing holosystolic murmur along the lower left sternal margin, which may be intensified during inspiration and reduced during expiration or with the Valsalva maneuver (Carvallo’s sign). This murmur is sometimes associated with a prominent right ventricular pulsation along the left parasternal region or regurgitant waves seen in the neck veins. Choice e is a murmur of aortic stenosis (AS). The murmur of AS is characteristically an ejection (mid) systolic murmur, low-pitched, rough and rasping in character, and loudest at the base of the heart, most commonly in the second right intercostal space and usually radiates upward along the carotid arteries.
An 82-year-old white woman is admitted to the hospital for observation after presenting to the emergency department with dizziness. After being placed on a cardiac monitor in the ER, the rhythm strip below was recorded. There is no past history of cardiac disease, diabetes, or hypertension. With prompting, the patient discloses several prior episodes of transient dizziness and one episode of brief syncope in the past. Physical examination is unremarkable. Which of the following is the best plan of care?
The patient in question has symptomatic tachycardia-bradycardia syndrome. Sinus node automaticity is suppressed by the tachyarrhythmia and results in a prolonged sinus pause following termination of the tachycardia. The patient in this case is symptomatic, and pacemaker placement is warranted; reassurance would put the patient at risk of further syncopal episodes and bodily harm from fall or accident. Although a pacemaker will prevent bradycardia, it does not prevent tachycardia. The patient may need medication to prevent tachycardia if she continues to be symptomatic after pacemaker placement. It is unlikely that any positive findings on a stress test could be correlated with her ECG findings. The tachy-brady syndrome does increase the patient’s risk of cardioembolic event, and anticoagulation should be considered. Aspirin, however, is not an appropriate agent to prevent cardiogenic embolism.
One month after hospital discharge for documented myocardial infarction, a 65-year-old man returns to your office concerned about low-grade fever and chest pain. He describes the chest pain as sharp, worse on deep inspiration and better when sitting up. He denies shortness of breath; his lungs are clear to auscultation. On your heart examination you do not appreciate any murmur or rubs. ECG is shown below. Which therapy is most likely to be effective in relieving his chest pain?
The patient has Dressler syndrome (post–myocardial infarction pericarditis), which may occur about 1 to 2 weeks post–myocardial infarction. It is thought to be an autoimmune phenomenon. The patient may have fever, leukocytosis, and pericardial or pleural effusion. The chest pain associated with pericarditis tends to be pleuritic and worse with sitting which places the pericardium closer to the chest wall. A pericardial friction rub is present in about 85% of patients. Typical ECG changes of pericarditis include diffuse ST-segment elevation. The characteristic PR-segment depression (opposite in polarity to the ST segment) due to a concomitant atrial injury current can also be appreciated in this patient. Acute ST elevation seen with myocardial infarction usually presents with regional or localized (as opposed to diffuse) ST elevation depending on the region of infarction (V1 -V4 in anteroseptal infarction; I, aVL, V5 , V6 in lateral infarction; and II, III, AVF in inferior infarction). Treatment of Dressler syndrome is the same as for other forms of pericarditis. A short course of a nonsteroidal anti-inflammatory agent or corticosteroids may help relieve symptoms. Anticoagulation is not a treatment for this condition, but, if needed for other indications, it should be used cautiously, since hemorrhagic pericarditis may result. A patient recently discharged from the hospital warrants suspicion of pneumonia, but this patient does not have other signs and symptoms suggesting pneumonia. Likewise the patient’s symptoms are not suggestive of anginal pain or panic attack, for which nitrates or anxiolytics might be prescribed.
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