Cardiovascular Board Review

A middle-aged man with progressive fatigue

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A 61-year-old white man presents with progressive fatigue, which began several months ago and has accelerated in severity over the past week. He says he has had no shortness of breath, chest pain, or symptoms of heart failure, but he has noticed a decrease in exertional capacity and now has trouble completing his daily 5-mile walk.

He saw his primary physician, who obtained an electrocardiogram that showed a new left bundle branch block. Transthoracic echocardiography indicated that his left ventricular ejection fraction, which was 60% a year earlier, was now 35%.

He has hypertension, dyslipidemia, type 2 diabetes, and chronic kidney disease. Although he was previously morbidly obese, he has lost more than 100 pounds with diet and exercise over the past 10 years. He also used to smoke; in fact, he has a 30-pack-year history, but he quit in 1987. He has a family history of premature coronary artery disease.

Physical examination. His heart rate is 75 beats per minute, blood pressure 142/85 mm Hg, and blood oxygen saturation 96% while breathing room air. He weighs 169 pounds (76.6 kg) and he is 6 feet tall (182.9 cm), so his body mass index is 22.9 kg/m2.

He is awake and in no acute distress. His breath sounds are normal, without crackles or wheezes. His heart has a normal rate and regular rhythm; he has normal first and second heart sounds and no extra sounds or murmurs; the apical impulse is not displaced. His abdomen is soft and nontender, with no hepatosplenomegaly or hepatojugular reflex. His extremities are warm and well perfused, with normal peripheral pulses and no edema. He has no gross neurologic defects.
Figure 1. The patient’s electrocardiogram shows sinus rhythm, rate 80 beats per minute, left-axis deviation, QRS duration 148 ms, a QS complex in lead V1 (black arrow), and monophasic R waves in leads I and V6 (red arrows). There are concordant T waves in leads V4 and V5 (blue arrows).
Initial laboratory analysis (Table 1) shows evidence of anemia and renal insufficiency and a slightly elevated serum level of glucose. His cardiac biomarkers are within normal limits, but his B-type natriuretic peptide level is 483 pg/mL (reference range < 100 pg/mL). His thyroid-stimulating hormone level is in the normal range.

Electrocardiography reveals sinus rhythm with a left bundle branch block and left axis deviation (Figure 1), which were not present 1 year ago.

Chest roentgenography is normal.

A WORRISOME PICTURE

1. Which of the following is associated with left bundle branch block?

  • Myocardial injury
  • Hypertension
  • Aortic stenosis
  • Intrinsic conduction system disease
  • All of the above

All of the above are true. For left bundle branch block to be diagnosed, the rhythm must be supraventricular and the QRS duration must be 120 ms or more. There should be a QS or RS complex in V1 and a monophasic R wave in I and V6. Also, the T wave should be deflected opposite the terminal deflection of the QRS complex. This is known as appropriate T-wave discordance with bundle branch block. A concordant T wave is nonspecific but suggests ischemia or myocardial infarction.

Potential causes of a new left bundle branch block include hypertension, acute myocardial infarction, aortic stenosis, and conduction system disease. A new left bundle branch block with a concomitant decrease in ejection fraction, especially in a patient with cardiac risk factors, is very worrisome, raising the possibility of ischemic heart disease.

MORE CARDIAC TESTING

The patient undergoes more cardiac testing.

Transthoracic echocardiography is done again. The left ventricle is normal in size, but the ejection fraction is 35%. In addition, stage 1 diastolic dysfunction (abnormal relaxation) and evidence of mechanical dyssynchrony (disruption in the normal sequence of activation and contraction of segments of the left ventricular wall) are seen. The right ventricle is normal in size and function. There is trivial mitral regurgitation and mild tricuspid regurgitation with normal right-sided pressures.

A gated rubidium-82 dipyridamole stress test yields no evidence of a fixed or reversible perfusion defect.

Left heart catheterization reveals angiographically normal coronary arteries.

Magnetic resonance imaging (MRI) shows a moderately hypertrophied left ventricle with moderately to severely depressed systolic function (left ventricular ejection fraction 27%). The left ventricle appears dyssynchronous. Delayed-enhancement imaging reveals patchy delayed enhancement in the basal septum and the basal inferolateral walls. These findings suggest cardiac sarcoidosis, with a sensitivity of nearly 100% and a specificity of approximately 78%.1

SARCOIDOSIS IS A MULTISYSTEM DISEASE

Sarcoidosis is a multisystem disease characterized by noncaseating granulomas. Almost any organ can be affected, but it most commonly involves the respiratory and lymphatic systems.2 Although infectious, environmental, and genetic factors have been implicated, the cause remains unknown. The prevalence is approximately 20 per 100,000, being higher in black3 and Japanese 4 populations.

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