A patient on the mend suddenly develops cardiovascular problems.
The patient, a 73-year-old white woman, was recuperating uneventfully from surgery for diverticular disease. Ms. C was on the rehabilitation unit, receiving physical therapy and doing well. Early one morning, as we entered her room during rounds, she took us by surprise when she complained of pressure in her chest and shortness of breath.
WHAT COULD THE PROBLEM BE?
While the resident began to formulate the diagnostic possibilities, we immediately gave the patient oxygen, a chewable 325-mg aspirin, and sublingual nitroglycerin, but these did not relieve her symptoms. Her vital signs were normal: BP 140/90 mm Hg, pulse 80 beats per minute, respiration rate 20 breaths per minute, and pulse oximetry 94% on room air. On auscultation, Ms. C’s lungs were clear. Her heart had a regular rate and rhythm; no murmurs or rubs were heard. Her abdomen was soft. Extremities demonstrated no edema.
Top on the resident’s list of differential diagnoses was acute MI. And because Ms. C was recovering from surgery, pulmonary embolism was under consideration. We also entertained thoughts of pneumothorax and acute panic attack.
An ECG showing massive ST elevation in the anterior lateral leads seemed to confirm our suspicion of acute MI, while at the same time ruling out pulmonary embolism and reducing the likelihood of panic attack.
A cardiologist took Ms. C directly to the catheterization lab, where a completely normal angiogram ruled out MI.
Ms. C had Tako-Tsubo cardiomyopathy, also known as stress-induced transient cardiomyopathy. Brief dysfunction of the left ventricle with ballooning of the apical portion during systole is typical and accounted for the ECG changes seen in our patient. The absence of CAD must be established, as it was by Ms. C’s normal angiogram.
A stressful event—either medical or emotional—is thought to cause a surge in catecholamines, which in susceptible individuals may trigger Tako-Tsubo cardiomyopathy. It is possible that high levels of catecholamines lead to microvascular spasm or dysfunction, resulting in a stunned myocardium.
Stress-induced cardiomyopathy is most commonly seen in postmenopausal women. Possible complications include tachyarrhythmias (ventricular fibrillation or ventricular tachycardia), pulmonary edema, cardiogenic shock, and left ventricular outflow tract obstruction.Four diagnostic criteria must be met to make a diagnosis of stress-induced cardiomyopathy:
1. Absence of obstructive CAD by angiography
2. New ST-segment elevation on the ECG
3. Absence of head trauma, intracranial bleed, hypertrophic cardiomyopathy, myocarditis, or pheochromocytoma, and
4. Transient dyskinesis of the ventricle in association with regional wall-motion dysfunction.
The diagnosis was confirmed by our patient’s typical ECG changes, mild elevation in cardiac enzymes, normal coronary arteries with apical dyskinesia noted on angiogram, and occurrence in a postmenopausal female.(Postmenopausal women account for 82%-100% of cases.) Signs and symptoms similar to Tako-Tsubo cardiomyopathy may also be seen in patients with cocaine abuse, Prinzmetal’s angina, and cardiac syndrome X, but Ms. C’s history and normal angiogram ruled out all of these.
Although the severity of the acute illness is alarming, Tako-Tsubo cardiomyopathy is a transient disorder with an excellent prognosis. Our patient’s symptoms resolved spontaneously after the cardiac catheterization. Lab results returned post resolution showed a slight elevation in troponin (2.11, normal 0.00-1.50), a finding consistent with stress-induced cardiomyopathy. This elevation is transient, however, and not as great as would be seen in an MI.
An echocardiogram the next day was normal.
SO WHAT CAUSED MS. C’S PROBLEMS?
Prior to onset of her symptoms, Ms. C had an argument with her husband. Verbal abuse had been a disturbing part of their relationship for many years but had worsened recently. We suggested counseling for them, but they declined.