Gene/Protein Disease Symptom Drug Enzyme Compound
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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many patients with hypertrophic cardiomyopathy (HC) have impaired left ventricular (LV) rapid diastolic filling. To quantitate the contribution of atrial systole to LV filling, we used radionuclide angiography to study 30 normal volunteers and 42 patients with HC before and after oral administration of verapamil (320 to 560 mg/day). LV time-activity curves were constructed by combined forward and reverse gating from the R wave, and the onset of atrial systole was determined by the P-R interval. The percent of LV stroke volume filled during rapid diastolic filling and atrial systole was then computed. Peak LV filling rate during rapid diastolic filling was expressed in end-diastolic volume (EDV)/second. Peak rate of rapid diastolic filling was not different in normal patients and those with HC (3.3 +/- 0.6 versus 3.3 +/- 1.1 EDV/s) and was within the normal range in 34 patients with HC (81%). However, the contribution to LV filling volume by rapid diastolic filling was diminished in patients with HC (83 +/- 7% normal, 67 +/- 17% HC, p less than 0.001) and the contribution of atrial systole was increased (16 +/- 8% normal, 31 +/- 18% HC, p less than 0.001). LV filling volume during atrial systole was above the upper normal limit of 31% in 17 patients (40%), including 13 patients with a normal peak filling rate. After verapamil, peak filling rate increased (to 4.2 +/- 1.2 EDV/s, p less than 0.001), percent LV filling during rapid diastolic filling increased (to 83 +/- 7%, p less than 0.001), and percent LV filling during atrial systole decreased (to 16 +/- 9%, p less than 0.001). Percent LV filling volume during atrial systole was abnormal after verapamil in only 3 patients (7%). Hence, although the peak rate of rapid diastolic filling may be normal in patients with HC, the contribution to LV filling by rapid diastolic filling is reduced and that of atrial systole is thereby increased. Increased rate and magnitude of rapid diastolic filling during verapamil is associated with decrease and normalization of the contribution of atrial systole to LV filling. These data suggest that many patients with HC are at risk of hemodynamic decompensation with the onset of atrial fibrillation or other tachyarrhythmias and loss of the atrial contribution to LV filling. This risk may be reduced during verapamil therapy.
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PMID:Atrial systole and left ventricular filling in hypertrophic cardiomyopathy: effect of verapamil. 668 16

To determine the hemodynamic effect of verapamil at rest and during exercise, 18 patients with hypertrophic cardiomyopathy were studied before and after 7 weeks of treatment with oral verapamil (maximal dose, 720 mg/day). At rest and at peak exercise, verapamil produced a significant increase in left ventricular (LV) systolic performance in terms of stroke volume index (rest, from 43 +/- 11 to 53 +/- 11 ml/m2, p less than 0.001; exercise, from 46 +/- 11 to 51 +/- 10 ml/m2, p less than 0.01), whereas heart rate decreased (rest, from 81 +/- 14 to 70 +/- 11 min-1, p less than 0.001; exercise, from 150 +/- 21 to 141 +/- 18 min-1, p less than 0.01). Cardiac index at rest and during exercise remained unchanged. Systolic vascular resistance did not change at rest, but decreased significantly during exercise (974 +/- 243 to 874 +/- 174 dynes s cm-5; p less than 0.05). After verapamil administration, pulmonary artery pressures did not change at rest, but decreased significantly during exercise. This was probably due to a shift in the LV pressure-volume relation. The improvement in LV hemodynamics was associated with a significant increase in exercise capacity. The findings of this study indicate that in patients with hypertrophic cardiomyopathy, hemodynamic improvement at rest and during exercise can be achieved by chronic administration of verapamil.
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PMID:Influence of verapamil therapy on left ventricular performance at rest and during exercise in hypertrophic cardiomyopathy. 668 88

To investigate the effects of verapamil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy, we studied 14 patients at catheterization with a nonimaging scintillation probe before and after serial intravenous infusions of low-, medium-, and high-dose verapamil (total dose 0.17 to 0.72 mg/kg). Percent change in radionuclide stroke counts after verapamil correlated well with percent change in thermodilution stroke volume (r = .87), and changes in diastolic and systolic counts were used to assess relative changes in left ventricular volumes after verapamil. Verapamil produced dose-related increases in end-diastolic counts (19 +/- 9% increase; p less than .001), end-systolic counts (91 +/- 54% increase; p less than .001), and stroke counts (7 +/- 10% increase; p less than .02). This was associated with a decrease in ejection fraction (83 +/- 8% control, 73 +/- 10% verapamil; p less than .001) and, in the 10 patients with left ventricular outflow tract gradients, a reduction in gradient (62 +/- 27 mm Hg control, 32 +/- 35 mm Hg verapamil; p less than .01). The end-systolic pressure-volume relation was shifted downward and rightward in all patients, suggesting a negative inotropic effect. In 10 patients, left ventricular pressure-volume loops were constructed with simultaneous micromanometer pressure recordings and the radionuclide time-activity curve. In five patients, verapamil shifted the diastolic pressure-volume curve downward and rightward, demonstrating improved pressure-volume relations despite the negative inotropic effect, and also increased the peak rate of rapid diastolic filling. In the other five patients, the diastolic pressure-volume relation was unaltered by verapamil, and increased end-diastolic volumes occurred at higher end-diastolic pressures; in these patients, the peak rate of left ventricular diastolic filling was not changed by verapamil. The negative inotropic effects of intravenous verapamil are potentially beneficial in patients with hypertrophic cardiomyopathy by decreasing left ventricular contractile function and increasing left ventricular volume. Verapamil also enhances left ventricular diastolic filling and improves diastolic pressure-volume relations in some patients despite its negative inotropic effect.
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PMID:Effects of verapamil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy: pressure-volume analysis with a nonimaging scintillation probe. 668 10

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.
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PMID:The effects of intraventricular gradients on left ventricular ejection dynamics. 668 40

Verapamil therapy improves exercise tolerance and decreases symptoms in many patients with both obstructive and nonobstructive forms of hypertrophic cardiomyopathy. These salutory clinical effects result from favorable modification by verapamil of the pathophysiologic abnormalities in left ventricular function characteristic of this disease: impaired early diastolic relaxation and filling, reduced end-diastolic volume and stroke volume, hypercontractile systolic function, and, in many patients, subvalvular outflow tract obstruction. The acute administration of intravenous verapamil produces both significant negative inotropic effects and significant effects on left ventricular diastolic function, resulting in reduced contractile state, diminished outflow gradient, increased end-diastolic volume and stroke volume and improved relaxation and diastolic filling. In some patients, one effect may predominate over the other, and improved diastolic function may be masked by the profound changes in systolic function. During short-term oral therapy, enhanced diastolic function is the predominant effect, although negative inotropic mechanisms are evident in some patients. These effects on left ventricular systolic and diastolic function persist during chronic oral verapamil therapy, contributing to the long-term clinical improvement experienced by many patients.
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PMID:The acute and chronic effects of verapamil on left ventricular function in patients with hypertrophic cardiomyopathy. 668 45

The diastolic function and the correlation between pump and diastolic function of left ventricle were studied in 35 patients with idiopathic hypertrophic cardiomyopathy with subaortic stenosis via a M-echocardiographic investigation by Echoview 80 C in the routine method. The following indices were used: A. For the diastolic function: 1. Telediastolic dimension (TDD) and volume (TDV) of left ventricular cavity. 2. Dimension (DPhFF) and volume (VPhFF) of the left ventricular cavity at the end of the phase of fast filling; 3. Velocity of fast filling of the left ventricle (ml/sec) - (formula; see text) 4. Fraction of fast filling of left ventricle (%) - (formula; see text) 5. Velocity of backward motion of the anterior mitral cusp at the beginning of diastole (E - F segment); 6. Velocity of early diastolic motion of the posterior wall of left ventricle (PWLV); 7. Ratio between early diastolic (D) and systolic (S) interval of PWLV: D/S; 8. Telediastolic interval (A - C) of mitral valve; 9. Index of fast emptying of left ventricle; 10. Amplitude E - E' of mitral echogram; II. Area (cm2) between two mitral cusps in diastole. B. For the systolic (pump) function: 1. Stroke and minute volume (SV, MV) of left ventricle according to the cubic formula and Teicholz formula; 2. Telesystolic dimension (TSD) and volume (TSV) of left ventricular cavity; 3. Fraction of shortening (FS) of left ventricle (%); 4. Mean velocity of shortening of the circumferential fibres (mVcf) of left ventricle (circumf./S); 5. Ejection fraction (EF) of left ventricle (%). 6. Distance between left ventricular endocardium of interventricular septum and point E of mitral valve; 7. Fraction of systolic thickening of IVS and PWLV; 8. Velocity of systolic thickening of IVS and PWLV; 9. Amplitude of systolic motion of IVS and PWLV.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diastolic and systolic functions of the left ventricle determined by M-echocardiography in idiopathic hypertrophic cardiomyopathy]. 668 23

We investigated left ventricular (LV) function in 40 patients (pts) with hypertension (HT), 16 pts with hypertrophic cardiomyopathy (HCM), 3 pts with ASH and HT and in 27 control subjects by M-mode echocardiography using supine exercise (50 watts, 3 minutes). The hypertensive subjects were echocardiographically divided into three subsets; the normal LV (17 cases), the hypertrophied LV (17 cases) and the dilated LV (6 cases). Similarly, pts with HCM were echocardiographically and cineangiographically divided into three subsets; ASH (asymmetric septal hypertrophy, 6 cases), APH (predominant apical hypertrophy, 6 cases) and DFH (diffuse left ventricular hypertrophy, 4 cases). Changes of left ventricular dimension Controls and HT: Stroke volume was increased during exercise in the controls, normal LV and hypertrophied LV groups by decreasing LV end-systolic dimension ( LVDs ), but it was increased in dilated LV group by increasing LV end-diastolic dimension ( LVDd ) (Frank-Starling mechanism). LVDd was increased transiently in the controls and normal LV group during recovery, but its grade and duration were more pronounced in the latter. LVDd did not change significantly in hypertrophied and the dilated LV groups. HCM: LVDd and LVDs did not change significantly during exercise in all 3 groups. LVDd was increased transiently during recovery in ASH group, but not in the other groups. Changes of peak velocity of circumferential fiber shortening (VCF) and the ratio of peak systolic blood pressure to LV end-systolic volume (PSP/ LVVs ). Controls and HT: Peak VCF was increased during exercise most markedly in the normal LV group, but it was not increased in the dilated LV group. PSP/ LVVs was increased significantly during exercise in the controls, the normal and hypertrophied LV groups, but not in the dilated LV group. HCM: Peak VCF showed a significant increase during exercise in ASH group, but not in the other two groups. Changes of the D/S ratio. The ratio of systolic to diastolic velocity of the LV posterior wall was expressed as a D/S. This ratio did not change significantly in the controls, HT and APH groups, but it was decreased significantly in ASH and DFH groups. LV end-systolic wall stress and LVDs relationship ( ESWst - LVDs ).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Exercise echocardiography in different types of hypertension classified by left ventricular geometry; comparison with hypertrophic cardiomyopathy]. 668 25

The effects of nifedipine on left-ventricular dynamics were assessed in 6 patients with hypertrophic obstructive cardiomyopathy (HOCM). After intravenous infusion of 3 mg nifedipine the mean aortic pressure decreased from 100 +/- 14 to 85 +/- 8 mm Hg (P less than 0.001). Heart rate increased from 70 +/- 5 to 93 +/- 5 beats per minute (P less than 0.001). This led to an increase of cardiac index from 3.0 +/- 0.5 to 3.8 +/- 0.9 l/min . m2 (P less than 0.01), whereas the stroke volume index decreased from an average of 49 +/- 11 to 42 +/- 12 ml/m2 (P less than 0.05). A marked diminution of outflow obstruction was demonstrable in 3 patients with intraventricular pressure gradients. The left-ventricular enddiastolic pressure rose from 14 +/- 3 to 18 +/- 6 mm Hg (P less than 0.02) in all patients. This effect was accompanied by a clear-cut coronary dilatation, evidenced by an increase of oxygen saturation in the coronary sinus from 29 +/- 4 to 54 +/- 9% (P less than 0.001). Thus nifedipine leads to diminished outflow obstruction and concomitant increase of cardiac output in hypertrophic cardiomyopathy. Inhibition of contraction does not seem to be compensated by peripheral effects. Coronary dilatation demonstrable in HOCM patients permits protection against coronary spasms and thus an additional antianginous effects.
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PMID:[Nifedipine in hypertrophic obstructive cardiomyopathy]. 689 Apr 38

We studied the dynamics of left ventricular (LV) emptying in 8 patients with asymmetric septal hypertrophy (ASH), 6 patients with concentric hypertrophic cardiomyopathy (CHC), and 6 normal controls. Four patients with ASH had resting systolic gradients greater than 20 mmHg, all had significant post premature ventricular contraction (PVC) systolic pressure gradients. LV volume (V) was obtained by frame-by-frame analysis of cineangiograms. End-diastolic volume was similar for all groups; end-systolic volume was significantly less in ASH and CHC patients than in normals. Maximum dV/dt was similar in ASH and CHC, and significantly greater than normals. Total systolic contraction time (SCT), i.e., time from peak volume to last cine frame at minimum volume, was similar for all groups, but the time required to eject 90% of stroke volume (90%T), as a fraction of SCT, was shorter for ASH (0.52 +/- 0.07) and CHC patients (0.51 +/- 0.05) than normals (0.67 +/- 0.07) (p less than 0.05 vs myopathy groups). In the sinus beat following a PVC, however, this ratio decreased significantly in normals and CHC patients, but did not change in ASH patients. We conclude that ASH and CHC have similar exaggerated systolic LV ejection dynamics in the basal state; the failure of ASH patients with post-PVC systolic outflow gradient to reduce 90% T/SCT post PVC may reflect obstruction to LV emptying.
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PMID:Left ventricular emptying dynamics in patients with asymmetric septal hypertrophy and concentric hypertrophic cardiomyopathy. 689 Dec 98

In the state of Connecticut, 233 women with congenital heart defects were prospectively followed up through 482 pregnancies that resulted in 372 infants who were examined frequently during their first 3 years of life. Approximately half of the women had undergone cardiac surgery and they were compared with the women without operation. There was no maternal mortality, and no patient had infective endocarditis, brain abscess or a cerebrovascular accident. The proportion of pregnancies resulting in live births did not differ significantly in mothers with and without cardiac surgery; the average live birth rate was 77 percent in all. However, the number and size of live-born infants was much greater in mothers who had become acyanotic as a result of reparative surgery than in the still cyanotic women, whether or not they had had palliative surgery. In cyanotic women, placental size was abnormally large in relation to birth weight, which was abnormally low. When the mothers were classified according to cardiac function, there was a significant difference between the number of infants born alive to mothers in good to excellent status and the number born to mothers in fair to poor condition. The latter had a significant increase in interrupted pregnancies as well as in cardiovascular complications during pregnancy. The total group had a 16.1 percent incidence rate of infants with congenital heart disease. This rate was corrected to 14.2 percent by removal of seven mothers, two with Noonan's syndrome, one with hypertrophic cardiomyopathy and four with a family history of congenital heart defects.
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PMID:Pregnancy and its outcome in women with and without surgical treatment of congenital heart disease. 711 41


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