Reversal of Acute Systolic Dysfunction and Cardiogenic Shock in Hypertrophic Cardiomyopathy by Surgical Relief of Obstruction

Sherrid, Mark V.; Balaran, Sandhya; Korzeniecki, Eva; Chaudhry, Farooq A.; Swistel, Daniel G.

doi:10.1111/j.1540-8175.2011.01459.x

Cited by 16 publications

(21 citation statements)

References 16 publications

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“…In patients with latent obstruction who suddenly develop a persistently high resting gradient, we have observed progressive LV systolic dysfunction and cardiogenic shock. Although some patients can be rescued with volume loading and negative inotropes 69 , we have seen several individuals in whom this spiral could be arrested only by surgical relief of obstruction 70 . These patients had systolic dysfunction that was disproportionate to the degree of ischaemia manifest on the electrocardiogram, and disproportionate to the minimal rise in cardiac biomarkers.…”

Section: [H3] Resting Wall Motion Abnormalitiesmentioning

confidence: 91%

Myocardial energy depletion and dynamic systolic dysfunction in hypertrophic cardiomyopathy

2016

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Evidence indicates that anatomical and physiological phenotypes of hypertrophic cardiomyopathy (HCM) stem from genetically mediated, inefficient cardiomyocyte energy utilization, and subsequent cellular energy depletion. However, HCM often presents clinically with normal left ventricular (LV) systolic function or hyperkinesia. If energy inefficiency is a feature of HCM, why is it not manifest as resting LV systolic dysfunction? In this Perspectives article, we focus on an idiosyncratic form of reversible systolic dysfunction provoked by LV obstruction that we have previously termed the 'lobster claw abnormality' — a mid-systolic drop in LV Doppler ejection velocities. In obstructive HCM, this drop explains the mid-systolic closure of the aortic valve, the bifid aortic pressure trace, and why patients cannot increase stroke volume with exercise. This phenomenon is characteristic of a broader phenomenon in HCM that we have termed dynamic systolic dysfunction. It underlies the development of apical aneurysms, and rare occurrence of cardiogenic shock after obstruction. We posit that dynamic systolic dysfunction is a manifestation of inefficient cardiomyocyte energy utilization. Systolic dysfunction is clinically inapparent at rest; however, it becomes overt through the mechanism of afterload mismatch when LV outflow obstruction is imposed. Energetic insufficiency is also present in nonobstructive HCM. This paradigm might suggest novel therapies. Other pathways that might be central to HCM, such as myofilament Ca2+ hypersensitivity, and enhanced late Na+ current, are discussed

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Section: [H3] Resting Wall Motion Abnormalitiesmentioning

confidence: 91%

Myocardial energy depletion and dynamic systolic dysfunction in hypertrophic cardiomyopathy

2016

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“…4,[8][9][10][11][12][13] It is most commonly manifest as a reversible mid-systolic drop in pulsed Doppler mid-LV ejection velocities and flow in patients with LVOT gradients >60 mm Hg; its characteristic spectral Doppler appearance has fostered the term the "lobster claw" abnormality. 4,[8][9][10][11][12][13] It is most commonly manifest as a reversible mid-systolic drop in pulsed Doppler mid-LV ejection velocities and flow in patients with LVOT gradients >60 mm Hg; its characteristic spectral Doppler appearance has fostered the term the "lobster claw" abnormality.…”

Section: Introductionmentioning

confidence: 99%

“…8,9 This flow abnormality is caused by a premature termination of longitudinal LV contraction. 12 Their dramatic clinical course led us to search our databases for other patients with apical ballooning in obstructive HCM. These two patients developed apical and mid-ventricular ballooning, refractory cardiogenic shock, and heart failure.…”

Section: Introductionmentioning

confidence: 99%

“…[8][9][10][11][12][13] There is no compelling need to posit another neurohumoral mechanism. [8][9][10][11][12][13] There is no compelling need to posit another neurohumoral mechanism.…”

mentioning

confidence: 99%

“…The specific surgical strategy for relief of left ventricular outflow obstruction should depend on local expertise and practice 12,20,26,46. Emergent surgical relief of obstruction should be considered when shock with poor tissue perfusion or pulmonary congestion persist despite high-dose intravenous beta blockade, copious intravenous fluids, and intravenous phenylephrine.…”

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Hypertrophic cardiomyopathy with dynamic obstruction and high left ventricular outflow gradients associated with paradoxical apical ballooning

et al. 2018

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Background: Acute left ventricular (LV) apical ballooning with normal coronary angiography occurs rarely in obstructive hypertrophic cardiomyopathy (OHCM); it may be associated with severe hemodynamic instability. Methods, Results:We searched for acute LV ballooning with apical hypokinesia/akinesia in databases of two HCM treatment programs. Diagnosis of OHCM was made by conventional criteria of LV hypertrophy in the absence of a clinical cause for hypertrophy and mitral-septal contact. Among 1519 patients, we observed acute LV ballooning in 13 (0.9%), associated with dynamic left ventricular outflow tract (LVOT) obstruction and high gradients, 92 ± 37 mm Hg, 10 female (77%), age 64 ± 7 years, LVEF 31.6 ± 10%. Septal hypertrophy was mild compared to that of the rest of our HCM cohort, 15 vs 20 mm (P < 0.00001). An elongated anterior mitral leaflet or anteriorly displaced papillary muscles occurred in 77%. Course was complicated by cardiogenic shock and heart failure in 5, and refractory heart failure in 1. High-dose beta-blockade was the mainstay of therapy. Three patients required urgent surgical relief of LVOT obstruction, 2 for refractory cardiogenic shock, and one for refractory heart failure. In the three patients, surgery immediately normalized refractory severe LV dysfunction, and immediately reversed cardiogenic shock and heart failure. All have normal LV systolic function at 45-month follow-up, and all have survived.Conclusions: Acute LV apical ballooning, associated with high dynamic LVOT gradients, may punctuate the course of obstructive HCM. The syndrome is important to recognize on echocardiography because it may be associated with profound reversible LV decompensation. K E Y W O R D S hypertrophic cardiomyopathy, left ventricular outflow obstruction, left ventricular systolic dysfunction

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Distinctive Hypertrophic Cardiomyopathy Anatomy and Obstructive Physiology in Patients Admitted With Takotsubo Syndrome

Sherrid

Riedy

Rosenzweig

et al. 2020

The American Journal of Cardiology

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Reversal of Acute Systolic Dysfunction and Cardiogenic Shock in Hypertrophic Cardiomyopathy by Surgical Relief of Obstruction

Cited by 16 publications

References 16 publications

Myocardial energy depletion and dynamic systolic dysfunction in hypertrophic cardiomyopathy

Myocardial energy depletion and dynamic systolic dysfunction in hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy with dynamic obstruction and high left ventricular outflow gradients associated with paradoxical apical ballooning

Distinctive Hypertrophic Cardiomyopathy Anatomy and Obstructive Physiology in Patients Admitted With Takotsubo Syndrome

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