Acute Left Ventricular Ballooning: Tools to Differentiate Hypertrophic Cardiomyopathy with Outflow Obstruction from Neurohumoral Takotsubo Syndrome

Figures

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  Fig. 1.. Central figure highlighting the pathophysiological, diagnostic, and management differences between patients presenting with acute apical ballooning due to Takotsubo syndrome (TTS) versus obstructive hypertrophic cardiomyopathy (HCM). LVOT, left ventricular outflow tract; LV, left ventricle; LHC, left heart catheterization; IV, intravenous; RAAS, renal-angiotensin-aldosterone system.

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  Fig. 2.. The cardiac loop and SAM of the mitral valve. Flow within the LV follows a U-turn redirection between the LV inflow and outflow tracts, and goes around the mitral valve. The close proximity of the LV inflow and outflow tracts makes this anatomy susceptible to small perturbations, resulting in SAM in vulnerable individuals. In obstructive HCM, the mitral valve is swept into the septum by the pushing force of flow, also known as flow drag. Flow originates from a posterior and lateral direction, redirected by the septal bulge. As it does so, flow catches the mitral valve from its ventricular aspect and sweeps it into the septum. Reproduced by permission of the authors [52]. SAM, systolic anterior motion; LV, left ventricle; HCM, hypertrophic cardiomyopathy.

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  Fig. 3.. HCM with mild asymmetric septal hypertrophy, LVOT obstruction, and acute apical ballooning syndrome. A 63-year-old woman was admitted with near-syncope, hypotension, and NSTEMI (troponin I of 0.64 ng/mL). Coronary arteries were angiographically normal. LV cineangiography revealed acute apical ballooning. Left heart catheterization revealed an aortic pressure of 89/51 with a gradient of 100 mmHg. Following intravenous metoprolol, the patient’s outflow tract gradient improved to 40 mmHg, and her BP improved to 105/80 mmHg. A stress TTE performed 22 months after presentation demonstrated normal LV wall motion and no resting gradient. Following stress, TTE revealed mitral-septal contact and a peak LVOT gradient of 81 mmHg. This patient had very mild septal thickening HCM with acute apical ballooning due to LVOT obstruction presenting clinically as TTS. After recovery of LV systolic function, she continued to have severe LVOT gradients provocable after exercise. (A) Echocardiogram performed on admission (systolic frame) revealed apical and mid-LV ballooning with severe hypokinesis (arrowheads) and mitral-septal contact (white arrow). (B) Color Doppler (systolic frame) demonstrated…

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  Fig. 4.. Left heart catheterization and peak-to-peak pressure tracings of the patient described in Fig. 3, obtained using a retrograde pullback approach. (A) Pullback method for LV and aortic pressure tracings demonstrate a 60 mmHg gradient across the LVOT. (B) Aortic pressure tracings in the catheterization laboratory demonstrate a hypotensive patient with a systemic blood pressure of 87/51 mmHg. (C) Given the concern for acute apical ballooning due to severe LVOT obstruction in HCM, the patient was administered IV metoprolol 15 mg. Fifteen minutes later, aortic pressure tracings demonstrate improved systemic blood pressures to 110/60 mmHg, as well as an improved LVOT gradient to 40 mmHg. LV, left ventricle; LVOT, left ventricular outflow tract; HCM, hypertrophic cardiomyopathy; IV, intravenous.