Disopyramide in hypertrophic cardiomyopathy. I. Hemodynamic assessment after intravenous administration

The hemodynamic effects of intravenous disopyramide were determined in 43 patients with hypertrophic cardiomyopathy and pressure gradients at rest (resting obstruction). The basal subaortic pressure gradient decreased in all patients by a mean of 61 mm Hg (range 16 to 123); in 35 patients the gradient was abolished (less than 20 mm Hg). The reduction in pressure gradient was achieved through a decrease in left ventricular systolic pressure, from 178 to 135 mm Hg (p less than 0.0001), and a rise in aortic systolic pressure, from 105 to 123 mm Hg (p less than 0.0001). Left ventricular ejection time was reduced from 326 to 273 ms (p less than 0.0001). Left ventricular end-diastolic pressure decreased from 19 to 16 mm Hg (p less than 0.0001). In a subgroup of 13 patients, cardiac output was unchanged after disopyramide, despite a prolongation of the pre-ejection period from 104 to 137 ms (p less than 0.0001) indicating a decrease in contractility. The maintenance of cardiac output, despite a decrease in contractility, may reflect a decrease in mitral regurgitation resulting from the reduction of systolic anterior motion of the mitral valve by disopyramide. These results indicate that disopyramide produces predictably favorable hemodynamic effects in patients with hypertrophic cardiomyopathy and resting obstruction to left ventricular outflow.     

Change of left atrial systolic pressure waveform in relation to left ventricular end-diastolic pressure

The relation between the left atrial systolic pressure waveform and left ventricular end-diastolic pressure was observed in 17 patients who underwent diagnostic cardiac catheterization. Left atrial pressure and left ventricular pressure were simultaneously recorded from a multisensor catheter before and during angiotensin infusion. Left ventricular systolic pressure and left ventricular end-diastolic pressure were 133 +/- 17 and 12.3 +/- 3.2 mm Hg, respectively, before angiotensin infusion and increased to 168 +/- 18 (p less than 0.01) and 19.4 +/- 4.5 mm Hg (p less than 0.01), respectively, during infusion. The left atrial systolic pressure curve consisted of two positive waves--a first wave (A) and a second wave (A'). The A and A' wave pressures were 11.6 +/- 2.3 and 10.2 +/- 3.9 mm Hg, respectively, before angiotensin infusion and 16.5 +/- 2.9 (p less than 0.01) and 18.1 +/- 4.7 mm Hg (p less than 0.01), respectively, during infusion. The ratio of A'/A of left atrial systolic pressure was 0.81 +/- 0.27 before angiotensin infusion and 1.08 +/- 0.14 (p less than 0.01) during infusion. The ratio of A' to A of left atrial systolic pressure was linearly related to left ventricular end-diastolic pressure before and during (p less than 0.01) angiotensin infusion. The amplitude of the A wave exceeded that of the A' wave at normal left ventricular end-diastolic pressures. However, as the left ventricular end-diastolic pressure increased either at rest or during angiotensin infusion, the amplitude of the A' wave increased and often exceeded that of the A wave. These results suggest that the second (A') wave might be attributed to the increased reflection associated with increased left ventricular end-diastolic pressure.     

Left ventricular function during stable sustained ventricular tachycardia. Hemodynamic and echo-Doppler analysis

To assess the left ventricular function during sustained stable ventricular tachycardia (VT), ten patients, aged 58 to 74, underwent simultaneous echo-Doppler and hemodynamic studies during sinus rhythm and induced sustained stable monomorphic VT. The VT cycle length was 447 +/- 92 ms (mean +/- SD). During VT, cardiac index fell from 2.32 +/- 0.54 to 1.62 +/- 0.63 L/min/m2 (p less than 0.001), and systemic systolic blood pressure fell from 129 +/- 18 to 107 +/- 18 mm Hg (p less than 0.001), while left ventricular end-diastolic pressure showed a rising trend from 9 +/- 7 to 15 +/- 12 mm Hg, and pulmonary artery wedge pressure rose from 10.2 +/- 1.6 to 24.2 +/- 2.3 mm Hg (p less than 0.005). By echo-Doppler the ejection fraction and the presence and degree of valvular regurgitation were not significantly changed during VT. The mean maximal left ventricular inflow tract velocities, mean time velocity integrals, and the mean time velocity integrals normalized for heart rate (measures of left ventricular diastolic filling) decreased from 0.59 +/- 0.074 to 0.40 +/- 0.053 m/s (p less than 0.05), from 0.12 +/- 0.029 to 0.021 +/- 0.012 m (p less than 0.001), and from 7.43 +/- 1.20 to 3.21 +/- 1.49 m x beats/min (p less than 0.001) during VT, respectively. We conclude that hemodynamic changes during stable sustained VT are neither associated with significant changes in systolic left ventricular function nor related to valvular regurgitation and are likely caused by impaired left ventricular diastolic filling.     

Diastolic function of the nonfilling human left ventricle.

OBJECTIVES. To investigate an early-diastolic left ventricular suction effect in humans, tip-micromanometer left ventricular pressure recordings were obtained in patients with mitral stenosis at the time of balloon inflations during percutaneous mitral valvuloplasty performed with a self-positioning Inoue balloon, which fits tightly in the mitral orifice. BACKGROUND. When mitral inflow was impeded in anesthetized dogs, left ventricular pressure decayed to a negative asymptote value. This negative asymptote value was consistent with an early diastolic suction effect. METHODS. Tip-micromanometer left ventricular pressure recordings were obtained in 23 patients with symptomatic mitral stenosis at the time of balloon inflations during percutaneous mitral valvuloplasty performed with a self-positioning Inoue balloon. RESULTS. The left ventricular diastolic asymptote pressure (P(asy)) was determined in 47 nonfilling beats with a sufficiently long (greater than 200 ms) diastolic time interval (that is, the interval from minimal first derivative of left ventricular pressure to left ventricular end-diastolic pressure) and equaled 2 +/- 3 mm Hg for beats with normal intraventricular conduction and 3 +/- 2 mm Hg for beats with aberrant intraventricular conduction. Left ventricular angiography was performed in five patients during the first inflation of the Inoue balloon at the time of complete balloon expansion. Left ventricular end-diastolic volume of the nonfilling beats averaged 38 +/- 14 ml and was comparable to the left ventricular end-systolic volume (39 +/- 19 ml) measured during baseline angiography before mitral valvuloplasty. Time constants of left ventricular pressure decay were calculated on 21 nonfilling beats with a diastolic time interval greater than 200 ms, normal intraventricular conduction and peak left ventricular pressure greater than 50 mm Hg. Time constants (T0 and TBF) derived from an exponential curve fit with zero asymptote pressure and with a best-fit asymptote pressure were compared with a time constant (T(asy)) derived from an exponential curve fit with the measured diastolic left ventricular asymptote pressure. The value for T(asy) (37 +/- 9 ms) was significantly smaller than that for TBF (68 +/- 28 ms, p less than 0.001) and the value for the measured diastolic left ventricular asymptote pressure (2 +/- 4 mm Hg) was significantly larger than that for the best-fit asymptote pressure (-9 +/- 11 mm Hg, p less than 0.001). T0 (44 +/- 20 ms) was significantly (p less than 0.01) different from TBF but not from T(asy). CONCLUSIONS. During balloon inflation of a self-positioning Inoue balloon, left ventricular pressure decayed continuously toward a positive asymptote value and left ventricular cavity volume was comparable to the left ventricular end-systolic volume of filling beats. In these nonfilling beats, the best-fit asymptote pressure was unrelated to the measured asymptote pressure and T0 was a better measure of T(asy) than was TBF. Reduced internal myocardial restoring forces, caused by different extracellular matrix of the human heart, reduced external myocardial restoring forces caused by low coronary perfusion pressure during the balloon inflation and inward motion of the balloon-occluded mitral valve into the left ventricular cavity could explain the failure to observe significant diastolic left ventricular suction in the human heart.     

Dynamic determinants of left ventricular early diastolic filling in old myocardial infarction.

The determinants of left ventricular early diastolic filling were assessed in 15 patients with old myocardial infarction. The left atrial pressure (LAP) and left ventricular pressure (LVP) were simultaneously measured by a Millar's multisensor micromanometer with the pusled Doppler mitral inflow velocity at baseline and during angiotensin infusion (20 ng/kg/min). Cardiac output was measured by a thermodilution method. LV peak systolic pressure and end-diastolic pressure were significantly (p less than 0.001) increased during angiotensin infusion from 137 +/- 19 to 170 +/- 21 mmHg and from 13.3 +/- 5.9 to 20.4 +/- 6.2 mmHg, respectively. Cardiac index was significantly decreased during angiotensin infusion. Heart rate, diastolic time, and peak positive dP/dt were unchanged. Although the LA-LV peak pressure gradient[(LAP-LVP) max] was unchanged (from 2.8 +/- 1.0 to 3.0 +/- 1.4 mmHg), the pressure gradient interval (the interval between the first and second points of transmitral pressure crossover) was significantly (p less than 0.001) decreased from 154 +/- 38 to 117 +/- 26 msec during angiotensin infusion. Peak early diastolic mitral inflow velocity (peak E) and the time-velocity integral of E wave (Ei) were significantly decreased during angiotensin infusion from 51 +/- 10 to 45 +/- 11 cm/sec (p less than 0.002) and from 7.47 +/- 1.96 to 5.70 +/- 1.66 cm (p less than 0.001), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of volume load of the left ventricle in aortic and mitral insufficiency on the geometry and function of the right ventricle

To investigate the effect of chronic left ventricular enlargement on right ventricular geometry and function, biplane cineventriculograms were analyzed in 23 patients with aortic regurgitation (AR) and in 17 patients with mitral regurgitation (MR). Left ventricular end-diastolic volume indices (LVEDVI) were elevated and significantly (p less than 0.05) different in patients with aortic regurgitation (AR) (190.2 +/- 65.2 ml/m2) and mitral regurgitation (MR) (148.7 +/- 40.1 ml/m2). Right ventricular end-diastolic volume indices (RVEDVI), however, were comparable and within the normal range (AR: 96.6 +/- 18.3 ml/m2, MR: 100.2 +/- 33.7 ml/m2). Mean pulmonary artery pressure was significantly (p less than 0.05) higher in patients with mitral regurgitation with 24.7 +/- 12.8 mm Hg (AR: 17.5 +/- 6.6 mm Hg). Six patients with mitral insufficiency had concomitant tricuspid valve insufficiency. In five out of six patients with tricuspid insufficiency, right ventricular afterload was significantly elevated. Only in patients with mitral regurgitation was a significant correlation (r) between left and right ventricular end-diastolic volume index found (RVEDVI = 0.7 X LVEDVI +1, r = 0.80). Moreover, in patients with MR, left ventricular end-diastolic volume index correlated with right ventricular end-systolic volume index (RVESVI = 0.4 X LVEDVI -8, r = 0.73). Right ventricular ejection fraction was significantly different (p less than 0.05) between patients with aortic and mitral insufficiency (AR: 53.7 +/- 8.9%, MR: 46.7 +/- 10.7%). Particularly in patients with normal left ventricular ejection fraction (greater than 50%) and mitral regurgitation, the incidence of a reduced right ventricular ejection fraction (less than 50%) was significantly higher (p less than 0.01) compared to patients with aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional mitral insufficiency in acute myocardial ischemia

In open-chest experiments in the dog, left ventricular failure was produced by serial ligation of branches of the left coronary artery. The evidence for left heart failure was (1) elevation of end-diastolic pressure of the left ventricle above a normal value of 10 to 12 mrn. Hg, and (2) increase of end-systolic volume. These hemo-dynamic changes preceded by many hours arterial hypotension or central venous hypertension.

Nine of 17 dogs with left heart failure presented hemodynamic and angiocardiographic evidence of significant degrees of mitral insufficiency. In all animals, mean left atrial and V wave pressures rose above control values. A systolic thrill was palpable over the distended left atrium. In three experiments the entire chamber of the left atrium became opacified after left ventricular injection. Left ventricular angiocardiography was more informative than the left atrial pressure for the detection of mitral insufficiency in the early stages of ventricular failure. Examination of the left atrial pressure curve appeared to be a more reliable index for quantitation of mitral reflux at late stages of heart failure. In the absence of any structural damage to the mitral valve in all the experiments, the resulting mitral insufficiency is described as functional.     

Regression of left ventricular mass is accompanied by improvement in rapid left ventricular filling following antihypertensive therapy with metoprolol

Left ventricular hypertrophy is associated with abnormal left ventricular diastolic filling in patients with hypertension. To assess the effects of antihypertensive therapy on the heart in nine previously untreated patients with echocardiographically-detected left ventricular hypertrophy, left ventricular mass and rapid left ventricular filling rate were compared before and after 6 months of treatment with metoprolol monotherapy. Metoprolol was given in doses of 100 to 400 mg/day (average dose, 167 mg/day in two divided doses) and significantly reduced both casual, office blood pressure (150/101 to 130/86 mm Hg, p less than 0.01) and 24-hour ambulatory blood pressure (139/91 to 126/79 mm Hg, p less than 0.05 for systolic, p less than 0.01 for diastolic). Following treatment with metoprolol, left ventricular mass index decreased from 135 +/- 20 to 120 +/- 13 gm/m2 (p less than 0.05), while rapid left ventricular filling rate increased from 1.89 +/- 0.24 to 2.09 +/- 0.27 end-diastolic volumes/sec (p less than 0.01). The reduction in left ventricular mass index was secondary to decreased posterior and septal wall thicknesses (13% and 11%, respectively, p less than 0.05 for both), as there were no changes in the left ventricular internal dimensions. Neither resting nor exercise left ventricular ejection fraction changed on metoprolol therapy compared to the baseline values. These data demonstrate that regression of left ventricular hypertrophy in never-previously-treated hypertensive patients is accompanied by improved diastolic performance following beta-adrenergic blocker monotherapy.     

Echocardiographic left ventricular mass and electrolyte intake predict arterial hypertension

OBJECTIVE: To identify predictors of arterial hypertension. PATIENTS: One hundred thirty-two normotensive adults from a large employed population. METHODS: Echocardiography, standard blood tests, and 24-hour urine collection, at baseline and after an interval of 3 to 6 years (mean, 4.7 +/- 0.8 years). RESULTS: At follow-up, 15 subjects (11%; 7 men, 8 women) had a systolic blood pressure greater than 140 mm Hg or a diastolic blood pressure greater than 90 mm Hg or both (mean, 143 +/- 7 and 87 +/- 6 mm Hg, respectively). At baseline, subjects who developed hypertension had a greater left ventricular mass index than those who did not (92 +/- 25 compared with 77 +/- 19 g/m2 body surface area; P less than 0.005) and higher 24-hour urinary sodium/potassium excretion ratio (3.6 +/- 1.7 compared with 2.6 +/- 1.4; P less than 0.04); there were no differences in race, initial age, systolic or diastolic blood pressure, coronary risk factors, or plasma renin activity. The likelihood of developing hypertension rose from 3% in the lowest quartile of sex-adjusted left ventricular mass index to 24% in the highest quartile (P less than 0.005); a parallel trend was less regular for quartiles of the sodium/potassium excretion ratio (P less than 0.04). In multivariate analyses, follow-up systolic pressures in all subjects and in the 117 who remained normotensive were predicted by initial age, systolic blood pressure, black race, and sex-adjusted left ventricular mass index; final diastolic blood pressure was predicted by its initial value, plasma triglyceride levels, urinary sodium/potassium ratio, low renin activity, black race, and plasma glucose level. CONCLUSIONS: Echocardiographic left ventricular mass in normotensive adults is directly related to the risk for developing subsequent hypertension. Left ventricular mass improves prediction of future systolic pressure, whereas diastolic pressure is more related to initial metabolic status. Black race is also an independent determinant of higher subsequent blood pressure.     

Left ventricular function in mitral valve stenosis]

In 12 patients with mitral stenosis left ventricular performance was assessed by pharmacologically (Methoxamine) induced increased afterload. At rest ventricular enddiastolic pressure (6.2 +/- 3.1 mm Hg), left ventricular enddiastolic volume (68 +/- 20 ml/m2), endsystolic volume (26 +/- 11 ml/m2) and left ventricular ejection fraction (0.63 +/- 0.06) were normal in each subject. Methoxamine induced a mean increment in peak systolic atrial pressure of 65 mm Hg. Left ventricular stroke volume, stroke work, stroke power, enddiastolic pressure and volume increased with Methoxamine in each patient. The mean left ventricular ejection fraction remained unchanged for the group and remained within the normal range for all patients. No difference was observed between the response of the mitral stenosis group and a control group of 10 normal subjects with the exception of the account of mitral regurgitation during the pressure load in 9 mitral stenosis patients. This study indicates the left ventricle in mitral stenosis is capable of a normal response to a pressure load. No evidence of impaired left ventricular function was detected in this group of patients.     

Use of a venous assist device after repair of complex lesions of the right heart

Sixteen patients underwent hemodynamic evaluation of a venous assist device after complex operations on the right side of the heart. The device consists of an inflatable abdominal binder attached to a Jobst extremity pump causing intermittent external compression of the abdomen. In addition, six of these patients were evaluated using total lower body compression for comparison. Modifications of the Fontan procedure were performed in 14 patients, mitral valve anuloplasty and tricuspid valve replacement in 1 patient and reconstruction of the right ventricular outflow tract for treatment of pulmonary atresia with intact septum in 1 patient. The patients' ages ranged from 23 months to 31 years (mean 10.7 +/- 1.8 years). Systemic blood pressure, right and left atrial pressures, heart rate and arterial-mixed venous oxygen saturation difference were recorded in each patient with and without the device in place. With the venous assist device, mean systolic pressure increased from 95 +/- 4 to 122 +/- 3 mm Hg (p less than 0.05) and diastolic pressure rose from 57 +/- 3 to 70 +/- 3 mm Hg (p less than 0.05). Left atrial pressure increased from 7 +/- 1 to 15 +/- 1 mm Hg and right atrial pressure from 15 +/- 1 to 23 +/- 1 mm Hg (both p less than 0.05). In addition, arterial-mixed venous oxygen saturation difference decreased from 29% without the device to 23% with the device in place (p less than 0.05). Total lower body compression gave similar results to intermittent abdominal compression alone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac consequences of renal transplantation: changes in left ventricular morphology and function

To characterize changes in left ventricular morphology and function associated with renal transplantation, noninvasive cardiac evaluations were performed in 41 adults at the time of surgery and at follow-up. At the time of transplantation, 36 patients had undergone hemodialysis through a fistula for 2.3 +/- 2.5 years (mean +/- SD); their hematocrit level was 26 +/- 6% and systolic blood pressure was 151 +/- 19 mm Hg. Perioperatively, left ventricular hypertrophy was present in 93% of patients by echocardiography, but in only 37% by electrocardiography. Abnormal left ventricular diastolic function was present in 67% of patients and indicated a high risk for perioperative pulmonary edema. At follow-up (1.5 +/- 1.4 years), mean hematocrit level increased to 39 +/- 7%, systolic blood pressure decreased to 132 +/- 14 mm Hg and spontaneous closure of the fistula occurred in 13 patients. Left ventricular mass by echocardiography decreased from 237 +/- 66 to 182 +/- 47 g (p less than 0.001), a decrease of 23%. Left ventricular volumes and cardiac index also decreased significantly, reflecting the rapid resolution of a pretransplant high output state. Despite proportionate regression of left ventricular hypertrophy within months of transplantation, diastolic function did not improve. The significant regression of left ventricular hypertrophy that occurs after renal transplantation may help explain the improved cardiovascular survival of patients with a renal transplant over that of patients on long-term dialysis.     

Left ventricular systolic and diastolic function in coronary artery disease: effects of revascularization on exercise-induced ischemia

Left ventricular systolic and diastolic function were studied before and after surgical revascularization in a group of 24 patients with stable angina who all had an excellent clinical response to surgery. With use of micromanometer left ventricular pressure measurements and ventricular volumes, calculated from biplane cineangiograms, left ventricular function at rest and during exercise before and after surgery was compared. Before surgery all patients had exercise-induced ischemia with new asynergy, a fall in ejection fraction from 57% to 49% (p less than .001), and a rise in left ventricular end-diastolic pressure from 23 to 37 mm Hg (p less than .001). Postoperative exercise resulted in no new asynergy and ejection fraction rose from 59% to 61% (p less than .05). Left ventricular end-diastolic pressure still rose from 17 to 25 mm Hg (p less than .01). Left ventricular pressure decay during exercise was greatly improved after revascularization and allowed maintenance of reduced early diastolic pressures. The early diastolic pressure nadir before surgery rose from 9 to 21 mm Hg (p less than .001); the postoperative nadir was 5 mm Hg at rest and 6 mm Hg during exercise. All patients had an upward shift in the diastolic pressure-volume relationship during preoperative exercise. After revascularization there was no upward shift in some patients and a much smaller shift in others. The postoperative increase in left ventricular end-diastolic pressure was due to increased end-diastolic volume, not altered compliance. There was an increase in mean right atrial pressure during exercise either before (6 to 11 mm Hg) or after surgery (4 to 10 mm Hg). These increases were quite variable, suggesting no consistent role of pericardial restraint during exercise. Early diastolic peak filling rate during exercise was greater after surgery (1260 vs 950 ml/sec, p less than .001). In fact, during postoperative exercise early diastolic filling rates were greater than normal, reflecting the persistence of abnormally high atrial pressures for filling. As at preoperative study, late diastolic filling during exercise was restricted after revascularization when compared with that in a control group. Postoperatively patients undergoing bypass procedures with a good clinical result showed significantly improved left ventricular diastolic and systolic function. Persistent elevation of end-diastolic and atrial pressures and other abnormalities of diastolic function may reflect chronic structural changes and need to be taken into account when evaluating patients after bypass surgery.     

Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: Altered left ventricular loading or improved muscle inactivation?

The calcium channel blocking agent, nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with hypertrophic cardiomyopathy. The mechanism of action of nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of nifedipine and the vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during nitroprusside infusion (132 +/- 38 mm Hg) and after nifedipine (132 +/- 32 mm Hg). During nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with nitroprusside, nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the calcium channel blocker, nifedipine, on diastolic mechanics in hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.     

Arterial hypertension and the right heart. A hemodynamic and echocardiographic study]

OBJECTIVE: To evaluate the effects of arterial hypertension on the pulmonary circulation and the right heart. SETTING: Coronary Care Unit (UTIC Arsénio Cordeiro) Hemodynamics Laboratory and Medicine I Echocardiography Laboratory-Santa Maria Hospital. PARTICIPANTS: 38 hypertensive patients separated in two groups: 24 with thickened septum and left ventricular posterior wall (10 with hemodynamic evaluation)--Group A--and 14 without thickening--Group B; a control group of 12 healthy volunteers--Group C. RESULTS: The hypertensive patients with hemodynamic evaluation had normal pulmonary capillary wedge pressure the average pulmonary resistance (135.29 +/- 63.47 dyn.cm.5), pulmonary systolic (31.30 +/- 10.01 mmHg) and mean pressures (18.23 +/- 8.21 mmHg) were raised, but the diastolic pulmonary pressure was normal. The right ventricle systolic pressure was raised (32.10 +/- 9.12 mmHg) and there was no modification of the right atrial or ventricular telediastolic pressures. On echocardiography there was a diastolic thickening of the right ventricular free wall in both group A (7.08 +/- 1.41 mm) and B (4.07 +/- 1.00 mm) as compared to group C (3.08 +/- 0.51 mm); there were similar findings regarding systolic thickness with statistical significance in group A (p less than 0.001). The right ventricular ejection fraction was normal in both groups. There was a positive correlation between the diastolic thickness of left ventricular posterior wall and right ventricular free wall in hypertensive patients and normotensive volunteers (r = 0.7754; p less than 0.001). CONCLUSIONS: The findings suggest an anatomic an functional relationship between both ventricles regarding the cardiac repercussions of arterial hypertension.     

Influence of preload changes on the filling function of the left heart ventricle studied by Doppler echocardiography

Left ventricular filling may be studied non-invasively by Doppler echocardiographic recording of transmitral blood flow. This study reports the variations in this flow induced by changing cardiac preload by administering trinitrin or by vascular filling in 27 patients undergoing catheterisation. Left ventricular end diastolic pressure (LVEDP) was measured by the pig-tail catheter used for ventriculography. Transmitral flow was recorded by pulsed Doppler using the apical view. The parameters studied were those of the early diastolic E wave and the end diastolic A wave. The hemodynamic and echocardiographic measurements were performed under basal conditions, after trinitrin and after vascular filling. Trinitrin was given to 14 patients and led to a fall in LVEDP from 17.6 +/- 4.5 to 6.7 +/- 1.4 mmHg (p less than 0.001). The amplitude of the mitral E wave decreased and the E/A ratio fell from 0.93 +/- 0.37 to 0.71 +/- 0.32 (p less than 0.001). Thirteen patients underwent vascular filling which increased LVEDP from 10.9 +/- 5 to 27 +/- 4 mmHg (p less than 0.001). The mitral E wave increased and the E/A ratio rose from 0.96 +/- 0.32 to 1.27 +/- 0.23 (p less than 0.01). The patients received trinitrin and then underwent vascular filling. The LVEDP decreased from 16 +/- 3.9 to 8 +/- 2.9 mmHg (p less than 0.001) and then rose to 28.3 +/- 3.5 mmHg (p less than 0.001). The E/A ratio fell after trinitrin from 0.91 +/- 0.40 to 0.58 +/- 0.30 (p less than 0.01) and then rose to 1.42 +/- 0.60 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of chronic pulmonary hypertension on left ventricular size, function, and interventricular septal motion

The effect of right ventricular pressure overload secondary to chronic pulmonary arterial hypertension on left ventricular size and function and on interventricular septal motion was studied in 13 patients in whom coronary artery disease, hypertension, and hypoxemia were excluded. Regional and global left ventricular function were assessed by computer-assisted analysis of two-dimensional directed M-mode echocardiograms obtained within 24 hours of a hemodynamic study. Septal position and motion were further analyzed by delineating seven points along the right and left sides of the septum during a single cardiac cycle. All echocardiographic data were compared to those of 10 normal subjects. Mean values for right ventricular systolic, mean pulmonary artery and pulmonary capillary wedge pressures were: 71 +/- 26 mm Hg, 46 +/- 16 mm Hg, and 7 +/- 1 mm Hg, respectively. Septal motion was interpreted from the M-mode echocardiograms as normal in seven patients (group I) and abnormal in the remaining six patients (group II). The only hemodynamic parameter which distinguished these two patterns was delta P, the transseptal systolic pressure gradient across the interventricular septum, which was significantly different (p less than 0.02) in group I (delta P = 65 +/- 16 mm Hg) from that of group II (delta P = 21 +/- 24 mm Hg). As a result of abnormal septal position, the septal-free wall dimensions of the left ventricle were reduced, but there was no evidence of depressed left ventricular performance in these patients. We conclude that resting left ventricular function is well preserved in patients with pulmonary hypertension, despite significant alterations in septal position and left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)     

Obstructive sleep apnea syndrome: more insights on structural and functional cardiac alterations, and the effects of treatment with continuous positive airway pressure.

OBJECTIVES: We studied structural and functional cardiac alterations in obstructive sleep apnea (OSA), their relationship to the severity of OSA, and the effects of treatment with continuous positive airway pressure (CPAP). BACKGROUND: Obstructive sleep apnea may influence the cardiac function by several mechanisms in the awake patient. METHODS: Left and right ventricular morphology and function were studied using echocardiography before and after treatment with CPAP in symptomatic patients (Epworth sleepiness score, 10 +/- 4.8) with severe OSA (apnea-hypopnea index [AHI], 42 +/- 24). The patients (n = 43, 32 men) had no known cardiac disease and were obese (body mass index, 31.6 +/- 5.4 kg/m2). The same echocardiographic parameters were studied in age-matched overweight patients (n = 40; body mass index, 26.4 +/- 2.3 kg/m2). RESULTS: The patients were hypertensive (systolic blood pressure, 153 +/- 25 mm Hg), with a higher resting heart rate (77 +/- 10 beats/min, p = 0.008) compared with age-matched control patients (n = 40). There was right ventricular dilatation, hypertrophic interventricular septum, reduced left ventricular stroke volume, tissue Doppler-determined systolic and diastolic velocities of the left and right ventricle, and normal pulmonary artery pressure. The structural and functional parameters were significantly associated with AHI (p < 0.004). Multiple stepwise regression showed the interventricular septum thickness, right ventricular free wall, and mitral annulus tissue Doppler systolic velocities to be predictive of a higher AHI (p < 0.001). Six months after treatment with CPAP, significant improvements were observed in the symptoms and hemodynamics, as well as left and right ventricular morphology and function. CONCLUSIONS: The structural and functional consequences of OSA on the heart are influenced by the severity of AHI. These effects are reversible if the apneic episodes are abolished.     

Altered left ventricular diastolic properties during pacing-induced angina in patients with aortic stenosis

An increase in left ventricular diastolic pressure has been repeatedly observed during angina in patients with coronary artery stenoses and regional demand ischemia, but the role of relaxation abnormalities versus left ventricular segmental dyssynchrony is controversial. In contrast, patients with angina due to aortic stenosis are likely to have diffuse rather than segmental ischemia and thus may provide an alternative model for examining the diastolic physiology of angina in man. Accordingly, we examined the hemodynamic manifestations of angina in eight patients with aortic stenosis without significant coronary artery disease. Angina was induced by pacing tachycardia, and hemodynamic and echocardiographic variables were measured in the control period and during angina in the beats immediately after cessation of pacing. Heart rate (control vs angina, 69 +/- 12 vs 70 +/- 11 beats/min, p = NS) and left ventricular peak systolic pressure (207 +/- 39 vs 222 +/- 22 mm Hg, p = NS) were similar in the control and postpacing angina periods. Left ventricular end-diastolic pressure, on the other hand, was significantly higher during postpacing angina (15 +/- 7 vs 28 +/- 8 mm Hg, p less than .01). The time constant of left ventricular pressure decline during isovolumetric relaxation (TL), calculated as the slope of a linear fit of the natural log of pressure vs time, increased from 44 +/- 5 to 51 +/- 7 msec (p less than .05); the time constant TD, derived from the slope of a linear fit of dP/dt vs pressure, also increased slightly, although the change was not statistically significant (69 +/- 5 vs 75 +/- 5 msec, p = .06).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of changes in airway pressure on the left ventricle and left atrium of dogs

The effects of negative and positive airway pressure were examined in eight closed chest, chronically instrumented dogs to determine beat to beat changes in left ventricular pressure, left ventricular dP/dt, left ventricular dimensions, and oesophageal pressure. As an index of afterload, systolic transmural pressure was calculated by subtracting oesophageal pressure from left ventricular pressure. With each change in airway pressure left ventricular end systolic minor axis diameter and left ventricular end diastolic minor axis diameter increased significantly. Left atrial end diastolic dimension increased significantly with negative airway pressure and did not change with positive airway pressure. Left ventricular dP/dt and left ventricular fractional shortening did not change. With the Mueller manoeuvre left ventricular systolic pressure decreased significantly from 106(4.2) mm Hg to 100.9(4.2) mm Hg and systolic transmural pressure increased significantly from 105.1(4.6) mm Hg to 110.4(4.3) mm Hg. With a transient increase in positive airway pressure of 30 mm Hg (4.0 kPa), left ventricular pressure increased significantly from 106.9(4.8) mm Hg to 113.9(5.9) mm Hg and systolic transmural pressure decreased significantly from 106.6(4.9) mm Hg to 99.8(4.6) mm Hg. The addition of positive end expiratory pressure of 10 cm H2O (0.98 kPa) or autonomic blockade with atropine and propranolol did not alter these results. Thus manoeuvres which cause opposite effects on systolic transmural pressure produce similar increases in left heart dimensions, suggesting that increases in pulmonary venous return and not changes in afterload may be the important determinants of left ventricular dimensional changes during changes in airway pressure.