Abstract:Echocardiographic and hemodynamic studies were obtained in 42 consecutive patients undergoing aortic valve replacement for isolated aortic stenosis. Concentric left ventricular (LV) wall thickening, the most common preoperative abnormality, occurred in 95% of patients. LV dilation with reduced fractional shortening was noted in approximately 25% of patients but was severe in only one patient. Six months after operation, LV wall thickness had decreased on average but had not returned to normal and fractional sh… Show more
“…Recent clinical observations of hypertrophy induced by volume (Clark et al, 1980) (Henry et al, 1980) overloads show that only a partial rather than full anatomical regression of ventricular enlargement follows replacement of an abnormal cardiac valve. The functional abnormalities associated with each hemodynamic overload also show only a partial reversal (Kennedy et al, 1977;Pantely et al, 1978).…”
SUMMARY. Chronic, progressive pressure overload of the cat right ventricle produces persistent, ongoing abnormalities of contractile, energetic, and biochemical function in vitro at a time when in vivo pump function is still normal. The present study tested the reversibility of the in vitro changes in this clinically relevant hypertrophy model. Fourteen sham-operated and 14 reversal cats were studied. After banding the animals as 1-kg kittens, right ventricular pressures were normal. Before band removal (25.2 ± 0.5 weeks later for the control group and 25.5 ± 0.3 weeks later for the hypertrophy reversal group), systolic right ventricular pressures were 24 ± 1 mm Hg for controls and 71 ± 5 mm Hg for the hypertrophy reversal group (P < 0.05). At study, 19.5 ± 1.1 weeks after a second sham operation for controls or 18.7 ± 0.7 weeks after band removal for the hypertrophy reversal group, these pressures were 24 ± 1 mm Hg for controls and 23 ± 1 mm Hg for the hypertrophy reversal group (P = NS); cardiac output was 0.18 ± 0.01 liters/kg per min for controls and 0.19 ± 0.01 liters/kg per min for the hypertrophy reversal group (P = NS). The ratio of right ventricle to body weight was normal in both groups, as was the right ventricular papillary muscle myocyte cross-sectional area and the myocardial collagen concentration. A right ventricular papillary muscle from each cat was studied at 29°C in a polarographic myograph. Preloaded shortening velocity was 0.79 ± 0.04 muscle lengths/sec for controls and 0.86 ± 0.03 muscle lengths/sec for the hypertrophy reversal group (P = NS); extent of shortening was 0.15 ± 0.01 muscle lengths for controls and 0.16 ± 0.01 muscle lengths for the hypertrophy reversal group (P = NS). At optimum isometric length, active tension was 59.7 ± 3 1 mN/mm for controls and 57.0 ±1.9 mN/mm 2 for the hypertrophy reversal group (P = NS); resting tension was 15.6 ±1.2 mN/mm 2 for controls and 13.6 ±1.6 mN/mm 2 for the hypertrophy reversal group (P = NS). Active and resting oxygen consumption levels did not differ in the two groups. This study demonstrates that-in the compensated stage of chronic, progressive pressure overload of the cat right ventricle-the contractile, energetic, and biochemical abnormalities of the hypertrophied myocardium are fully reversible. (Circ Res 54: 323-331, 1984)
“…Recent clinical observations of hypertrophy induced by volume (Clark et al, 1980) (Henry et al, 1980) overloads show that only a partial rather than full anatomical regression of ventricular enlargement follows replacement of an abnormal cardiac valve. The functional abnormalities associated with each hemodynamic overload also show only a partial reversal (Kennedy et al, 1977;Pantely et al, 1978).…”
SUMMARY. Chronic, progressive pressure overload of the cat right ventricle produces persistent, ongoing abnormalities of contractile, energetic, and biochemical function in vitro at a time when in vivo pump function is still normal. The present study tested the reversibility of the in vitro changes in this clinically relevant hypertrophy model. Fourteen sham-operated and 14 reversal cats were studied. After banding the animals as 1-kg kittens, right ventricular pressures were normal. Before band removal (25.2 ± 0.5 weeks later for the control group and 25.5 ± 0.3 weeks later for the hypertrophy reversal group), systolic right ventricular pressures were 24 ± 1 mm Hg for controls and 71 ± 5 mm Hg for the hypertrophy reversal group (P < 0.05). At study, 19.5 ± 1.1 weeks after a second sham operation for controls or 18.7 ± 0.7 weeks after band removal for the hypertrophy reversal group, these pressures were 24 ± 1 mm Hg for controls and 23 ± 1 mm Hg for the hypertrophy reversal group (P = NS); cardiac output was 0.18 ± 0.01 liters/kg per min for controls and 0.19 ± 0.01 liters/kg per min for the hypertrophy reversal group (P = NS). The ratio of right ventricle to body weight was normal in both groups, as was the right ventricular papillary muscle myocyte cross-sectional area and the myocardial collagen concentration. A right ventricular papillary muscle from each cat was studied at 29°C in a polarographic myograph. Preloaded shortening velocity was 0.79 ± 0.04 muscle lengths/sec for controls and 0.86 ± 0.03 muscle lengths/sec for the hypertrophy reversal group (P = NS); extent of shortening was 0.15 ± 0.01 muscle lengths for controls and 0.16 ± 0.01 muscle lengths for the hypertrophy reversal group (P = NS). At optimum isometric length, active tension was 59.7 ± 3 1 mN/mm for controls and 57.0 ±1.9 mN/mm 2 for the hypertrophy reversal group (P = NS); resting tension was 15.6 ±1.2 mN/mm 2 for controls and 13.6 ±1.6 mN/mm 2 for the hypertrophy reversal group (P = NS). Active and resting oxygen consumption levels did not differ in the two groups. This study demonstrates that-in the compensated stage of chronic, progressive pressure overload of the cat right ventricle-the contractile, energetic, and biochemical abnormalities of the hypertrophied myocardium are fully reversible. (Circ Res 54: 323-331, 1984)
“…'I--3 Aortic valvular stenosis can coexist with various types of subvalvular obstruction.2-14A9 These associated lesions cannot always be demonstrated angiographically, even by left ventriculography in several views. In such cases, obstructive lesions are best diagnosed from pressure gradients detected by catheter pullback from the ventricle to the proximal aorta.2 3, 10, 12, 19 Persistence or recurrence of intraventricular gradients shown by repeated or serial postoperative catheterization signals inadequate resection or regrowth of subvalvular obstructive lesions and possibly the need for further surgical resection.6 [20][21][22][23][24][25] Clinical investigation of normal ejection dynamics has shown that dynamic factors associated with flow contribute to physiologic transvalvular pressure gradients.26 Studies of flow dynamics in hypertrophic cardiomyopathy have cast strong doubt on the premise that large intraventricular pressure gradients are always a consequence of an anatomic obstruction of the outflow tract region.27 Improved instrumentation for measuring pressure28 33 has led to the frequent observation of subvalvular gradients in patients with valvular aortic stenosis without subvalvular pathology in our *The term gradients in this paper is used in the conventional hemodynamic sense, but in fluid dynamic terms represents a driving pressure difference evaluated across a finite distance in the direction of flow.
…”
SUMMARY Analysis of a tapering, pulsatile flow field predicts that substantial subvaivular pressure gradients exist in patients with valvular aortic stenosis (AS) without invoking a second anatomic site of obstruction. Using a catheter with two laterally mounted micromanometers, we examined the left ventricle in 11 patients with AS, mean age 64 ± 11 years (± SD); the mean valve area was 1.0 ± 0.3 cm2. Simultaneous measurements were made in (1) the left ventricular (LV) chamber and the LV outflow tract (LVOT) and (2) the LVOT and ascending aorta (AO). No patient had anatomic evidence of a subvalvular obstruction, but large subvalvular gradients were present in all. The average peak LV-LVOT and LV-AO gradients were 41 ± 17 mm Hg and 58 ± 23 mm Hg, respectively. Flow velocity was electromagnetically derived in two patients. The LV-LVOT gradient was associated with an increased flow velocity in the LVOT. This study suggests that large subvalvular gradients are present in AS and help overcome blood's inertia to convective and local accelerations in the tapering subvalvular flow field.SUBSTANTIAL intraventricular pressure differences and gradients* are traditionally considered to reflect an organic "outflow obstruction" in the region across which they are measured.1-9 It is commonly postulated that organic obstructions can be fixed or dynamic, and range from the collar type to the hypertrophic cardiomyopathy variants of subvalvular stenosis.'I--3 Aortic valvular stenosis can coexist with various types of subvalvular obstruction.2-14A9 These associated lesions cannot always be demonstrated angiographically, even by left ventriculography in several views. In such cases, obstructive lesions are best diagnosed from pressure gradients detected by catheter pullback from the ventricle to the proximal aorta.2 3, 10, 12, 19 Persistence or recurrence of intraventricular gradients shown by repeated or serial postoperative catheterization signals inadequate resection or regrowth of subvalvular obstructive lesions and possibly the need for further surgical resection.6 [20][21][22][23][24][25] Clinical investigation of normal ejection dynamics has shown that dynamic factors associated with flow contribute to physiologic transvalvular pressure gradients.26 Studies of flow dynamics in hypertrophic cardiomyopathy have cast strong doubt on the premise that large intraventricular pressure gradients are always a consequence of an anatomic obstruction of the outflow tract region.27 Improved instrumentation for measuring pressure28 33 has led to the frequent observation of subvalvular gradients in patients with valvular aortic stenosis without subvalvular pathology in our *The term gradients in this paper is used in the conventional hemodynamic sense, but in fluid dynamic terms represents a driving pressure difference evaluated across a finite distance in the direction of flow.
“…Moreover, when valve replacement is per formed because symptoms have developed, long-term postoperative survival is excellent: in our prospective natural history/prognosis series, survival during an average 4.4 years after operation was 83%. Late postoperative mortality, which was largely related to pros thesis-mediated complications or to coexist ing coronary artery disease, was not predicted by any objective functional characteristic [87]. Therefore, it would appear that symp tom status generally is an excellent indicator as to the appropriate timing of valve replace ment in the patient with aortic stenosis: when valve replacement is undertaken at the time of symptom onset, symptoms almost always are relieved, irreversible left ventricular dys function generally does not occur, and post operative prognosis is excellent.…”
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