Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (46 page)

Suggested Readings

Ben-Horin S, Bank I, Shinfeld A, et al. Diagnostic value of the biochemical composition of pericardial effusions in patients undergoing pericardiocentesis.
Am J Cardiol.
2007;99:1294–1297.

Hidron A, Vogenthaler N, Santos-Preciado JI, et al. Cardiac involvement with parasitic infections.
Clin Microbiol Rev.
2010;23:324–349.

Lange RA, Hillis D. Acute pericarditis.
N Engl J Med.
2004;351:2195–2202.

Levy PY, Cory R, Berger P, et al. Etiologic diagnosis of 204 pericardial effusions.
Medicine (Baltimore).
2003;82:385–391.

CHEST PAIN: HYPERADRENERGIC STATES

   Syndromes of catecholamine excess may cause chest pain from increased heart rate and peripheral vasoconstriction, resulting in a mismatch of oxygen supply and demand. Severe presentations may result in type 2 MI.

   Autoregulation of tissue blood flow and cardiac output are able to adapt to a wide range of perturbations in hear rate and blood pressure, particularly those that are chronic in nature. Symptoms are more likely to occur during periods of acute changes induced by either exogenous administration of catecholamines (cocaine, methamphetamines) or intrinsic paroxysmal episodes (stress cardiomyopathy, pheochromocytoma).

   Definition

   
Cocaine intoxication
: Chest pain is the most common reason for cocaine users to seek medical attention with 64,000 ED visits per year in the United States (50% admitted). Six percent of chest pain episodes are MI. Aortic dissection is a rare consequence of cocaine use. Cocaine is both sympathomimetic and thrombogenic and accelerates atherosclerotic deposition—as a result, ischemic damage can manifest as either type I MI (ruptured plaque) or type 2 MI (either severe epicardial spasm or increased oxygen demand).

   
Methamphetamine intoxication
: Biologic effects are similar to cocaine but with less vasoconstriction; more likely to produce tachyarrhythmias rather than chest pain.

   
Pheochromocytoma
: A rare form of secondary hypertension in 0.05% of hypertensive patients. It should be considered in patients with chest pain who lack coronary risk factors and who have characteristic symptoms or who worsen after beta-blocker administration (must rule out cocaine ingestion) (see Chapter
6
, Endocrine Diseases).

   
Stress-induced (takostubo) cardiomyopathy
: Transient dysfunction of the LV apex and/or mid-ventricle that mimics acute MI but is without obstructive coronary disease or clear epicardial (LAD) spasm. Pathogenesis is uncertain but likely is catecholamine mediated as it is often triggered by acute medical illness or emotional stress, occurs in the context of significantly elevated plasma catecholamines and mimics LV dysfunction seen in other hyperadrenergic states such as pheochromocytoma, neurologic injury, and exogenous administration of supraphysiologic doses of catecholamines (iatrogenic or intentional). Potentially mediated through direct toxic effect causing myocyte stunning or microvascular spasm. In several large registries, stress-induced cardiomyopathy accounts for 1–2% of all ACS inpatient admissions.

   Who Should Be Suspected?

   Often indistinguishable from symptoms of ACS, a hyperadrenergic etiology of chest pain should be a diagnosis of exclusion. In young individuals without coronary risk factors, cocaine exposure should be assessed immediately (beta-blockade therapy contraindicated).

   Stress-induced cardiomyopathy has a predilection for postmenopausal women for unclear reasons, although men are affected at a much lower rate. Early genetic studies have not yielded any polymorphism associated with the disease. Prevalence is 1–2% of hospital admissions for ACS. It should be suspected in postmenopausal women with ACS after a physical or emotional stressor with clinical presentation or ECG findings out of proportion to cardiac biomarker elevation.