Two Cases of Apical Ballooning Syndrome Masking Apical Hypertrophic Cardiomyopathy

Abstract

Apical akinesis and dilation in the absence of obstructive coronary artery disease is a typical feature of stress-induced (takotsubo) cardiomyopathy, whereas apical hypertrophy isS tress-induced cardiomyopathy involving akinesis of the left ventricular (LV) apex can mimic acute coronary syndrome but typically lacks obstructive coronary artery disease (CAD).1 Regional wall-motion abnormalities are usually transient, and the overall prognosis is favorable. Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder that can be localized in the LV apex. 2 We describe the cases of 2 patients whose diagnoses of apical-variant HCM were initially masked by their presentations with apical ballooning. Case Reports Patient 1In June 2011, a 43-year-old white woman with a history of alcohol abuse emergently presented with confusion, agitation, and shortness of breath of 2 days' duration. She had discontinued alcohol use and metoprolol succinate therapy 3 days before presentation. Her medical history included hypertension, previous tobacco use, and alcoholrelated liver disease. She had no known coronary disease. Her temperature was 36.7 °C; heart rate, 125 beats/min; blood pressure, 100/64 mmHg; respiratory rate, 34 breaths/min; and oxygen saturation, 96% on room air. Physical examination revealed tachycardia, non-tender hepatomegaly, and mild pitting edema in the lower extremities. The patient was confused, disoriented, and irritable without focal neurologic deficits.An electrocardiogram (ECG) showed sinus tachycardia with T-wave inversions and nonspecific ST-T-wave abnormalities in the anterolateral leads. Laboratory results included an elevated troponin T level of 0.27 ng/mL (normal, <0.03 ng/mL) and normal renal function. A transthoracic echocardiogram (TTE) showed an LV ejection fraction (LVEF) of 0.47 with hyperdynamic basal function but with a dilated, akinetic apex that suggested an apical variant of stress-induced cardiomyopathy (Fig. 1).

Transient apical wall thickening in patients with stress cardiomyopathy: Prevalence, profile, and impact on clinical course

“…We have observed this finding in several patients with SCM during recovery. There have also been several case reports regarding this phenomenon [9][10][11][12]; however, the incidence and clinical significance of this finding had not been studied. The results Data are expressed as number (%) or mean ± standard deviation.…”

“…Although reports on SCM are increasing, the nature of SCM remains ill-defined. Recently, transient apical wall thickening (TAWT), which mimics apical hypertrophic cardiomyopathy during recovery from SCM, has been reported [9][10][11][12]. This phenomenon developed during recovery of SCM patients who showed a marked increase in LV apical wall thickness that subsequently resolved [9][10][11][12].…”

Takotsubo cardiomyopathy resulting from exacerbation of chronic pancreatitis

“…Besides the causes of TCM presented above, also acute pancreatitis (via exaggeration of sympathetic stimulation that leads to transient myocardial dysfunction and microvascular hypoperfusion distributive shock) could act as a trigger for TCM. To date, only a few cases of acute pancreatitis induced TCM have been described [5][6][7]. We present, to the best of our knowledge, first case report of TCM resulting from the exacerbation of chronic pancreatitis.…”

Apical hypertrophic cardiomyopathy, a review of presentation, pathophysiology, diagnosis and natural course of the disease

“…18 In such cases TTE with contrast can be helpful. 18 Figure 3A shows typical findings on TTE in Takotsubo cardiomyopathy. TTE with contrast can also help in differentiating LV thrombus and LV non-compaction from AHCM.…”

“…TTE with contrast can also help in differentiating LV thrombus and LV non-compaction from AHCM. 18 Figure 3B and 3C show representative images of typical findings on TTE in LV thrombus and LV non compaction respectively. TTE with contrast can help in diagnosing AHCM in patients with high suspicion and a non-diagnostic TTE.…”