The effects of intraventricular gradients on left ventricular ejection dynamics

Abstract

The generation of abnormal gradients between the apical cavity and the subaortic valvular region of the left ventricle in patients with hypertrophic cardiomyopathy (HCM) has traditionally been equated to a dynamic obstruction to left ventricular outflow. To examine this concept in more detail, left ventricular ejection dynamics were studied during cardiac catheterization in 30 patients with HCM and 29 patients with no evidence of cardiovascular disease. Using multisensor catheterization techniques, ascending aortic flow velocity and micromanometer left ventricular and aortic pressures were simultaneously recorded during rest (n = 47). Dynamic left ventricular emptying was also analyzed with frame-by-frame angiography (n = 46). The temporal distribution of left ventricular outflow was independently derived from both flow velocity and angiographic techniques. The HCM patients were subdivided into three groups: I, intraventricular gradients at rest (n = 9); II, intraventricular gradients only with provocation (n = 12); III, no intraventricular gradients despite provocation (n = 9). Expressed as a precentage of the available systolic ejection period (%SEP), the time required for ejection of the total stroke volume was (mean +/- 1 S.D.): Group I, 69 +/- 17% (flow), 64 +/- 6% (angio); Group II, 63 +/- 14% (flow), 65 +/- 6% (angio); Group III, 61 +/- 16% (flow), 62 +/- 4% (angio); control group, 90 +/- 5% (flow) 86 +/- 10% (angio). No significant difference was observed between any of the three HCM subgroups, but, compared with the control group, ejection was completed much earlier in systole independent of the presence or absence of intraventricular gradients. The presence of coexisting mitral regurgitation in 12 of the HCM patients did not alter these results. This study demonstrates that 'outflow obstruction', as traditionally defined by the presence of an abnormal intraventricular pressure gradient and systolic anterior motion of the mitral valve, does not impede left ventricular outflow in HCM. In a pure fluid dynamic sense, we believe that outflow obstruction does not exist in this disease entity.

Postprandial Hemodynamics in Hypertrophic Cardiomyopathy

“…The occurrence of PPS in patients with HCM has been well known for many years, with patients frequently reporting symptoms of dynamic LVOT obstruction and a lower quality of life . Although the existence of dynamic LVOT obstruction in HCM was initially contested in the literature, several landmark studies have confirmed it as a true hemodynamic phenomenon with clinically significant consequences . In this study, we sought to demonstrate these hemodynamic changes in the HCM population with PPS using a resting, supine, 2‐dimensional Doppler echocardiography protocol before and after a standardized meal.…”

Pulmonary artery stiffness in fetuses with tetralogy of Fallot

“…This research showed that AcT influenced PAS to a greater extent than the MFV. Decreased pulmonary artery distensibility shortens the RV–pulmonary artery systolic ejection time (ET) [ 21 ]. In other words, the AcT of the pulmonary blood flow trace is shorter in fetuses with increased PAS.…”

Symptomatic Exercise-induced Intraventricular Gradient in Competitive Athlete

“… a) Increase of physiological non-obstructive IVGs; b) End-systolic obstruction secondary to ventricular cavity obliteration; c) Mid-systolic obstruction due to systolic anterior motion of the mitral valve with restriction of ejection flow. 3 , 4 …”

“…c) Mid-systolic obstruction due to systolic anterior motion of the mitral valve with restriction of ejection flow. 3 , 4 …”