Effect of percutaneous balloon valvuloplasty on pulmonary hypertension in mitral stenosis.

Percutaneous mitral balloon valvuloplasty (PMBV) has been useful in decreasing mitral valve obstruction in mitral stenosis; however, the long-term effects of valvuloplasty on pulmonary artery pressure have not been extensively studied. Thirty-three patients underwent PMBV in our institution between January 1988 and December 1991. There were significant reductions in peak (19 +/- 1 to 12 +/- 1 mm Hg) and mean (10 +/- 0.7 to 6 +/- 0.4 mm Hg) mitral valve gradients estimated by Doppler techniques immediately after PMBV. The mitral valve area, as assessed by the pressure half-time method, increased from 1.06 +/- 0.05 to 1.98 +/- 0.08 cm2 (p < 0.001) after the procedure and remained significantly greater (1.68 +/- 0.11 cm2) at 17 +/- 2 months. Right ventricular systolic pressure (RVSP) was estimated in patients with tricuspid regurgitation (TR) using the modified Bernoulli equation. There was a good correlation between Doppler and catheterization for RVSP (r = 0.83 pre valvuloplasty; r = 0.87 post valvuloplasty). Right ventricular systolic pressure by Doppler was 56 +/- 4 mm Hg before valvuloplasty and 48 +/- 4 mm Hg immediately afterwards (p < 0.001). Nine patients had TR on follow-up Doppler studies with an estimated RVSP of 53 +/- 9 mm Hg (p = NS compared with pre- and post-valvuloplasty values). Six of these nine patients had moderate or severe mitral regurgitation (MR), compared with one patient without TR at follow-up (p < 0.05). There appears to be a good correlation between the RVSP determined by Doppler and measured at catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)

Accuracy of subjective and computer-assisted assessments of angiographic left ventricular regional wall motion.

To evaluate the accuracy of angiographic methods for analysis of left ventricular regional wall motion, we measured the ability of a carefully performed subjective analysis (three independent observers) and that of three computer-assisted methods (centerline, radial, and area) to detect the presence of significant coronary artery disease. Normal ranges were established in 90 studies showing normal wall motion, and accuracy was tested in a second, consecutive series of 43 ventriculograms. The results show that the subjective method best separated those regions with from those without significant coronary disease. The subjective method also demonstrated sensitivity comparable to the centerline and radial methods. Among the computer-assisted methods, the area method was least sensitive but most specific for both anterior and inferior region coronary disease. The centerline and radial methods were highly sensitive, but less specific. When coronary disease was defined by electrocardiographic Q-waves, the area method had superior accuracy. Further analysis showed the following: 1) For the centerline and radial methods, long-axis reregistration of the end-systolic frame resulted in loss of sensitivity but increased specificity for anterior wall coronary disease, and little change in analysis of the inferior wall; 2) inclusion or exclusion of the apex had little effect on predictive accuracy for anterior wall coronary disease; 3) as expected, sensitivity and specificity results of all methods were dependent on the selection of a normal range cutoff value; but when performance was optimized, the subjective and area methods had a higher overall predictive accuracy than the centerline method; 4) It is likely that all three computer-assisted methods could be calibrated to give indications of degrees of hypokinesis, as their results correlated well with subjective observers' evaluations over the entire range of scores. These results should assist in selection of the optimal method for regional wall motion analysis in clinical and research applications. As currently applied, the area method is the most specific of the computer-assisted methods tested; the centerline and radial methods have highest sensitivity and therefore are most suited to detection of mild degrees of hypokinesis.

The M-Heart percutaneous balloon mitral Valvuloplasty Registry: initial results and early follow-up. The M-Heart Group.

The initial results, complications and early follow-up of 74 patients undergoing percutaneous balloon mitral valvuloplasty in seven hospitals participating in a multicenter registry are reported. Seventy-four patients with a mean age of 53 years had 75 valvuloplasty procedures performed over a 2.5 year period. Eighty-nine percent of the attempted procedures were completed and resulted in an increase in mean mitral valve area from 1.0 +/- 0.04 to 2.0 +/- 0.1 cm2 (p less than 0.0001); the valve area increased greater than or equal to 50% of the baseline valve area in 73% of the patients. Major complications included procedure-related death (2.7%), cardiac tamponade (6.7%), systemic embolism (2.7%) and emergency surgery (6.7%). At a mean follow-up period of 14.6 months, the condition of the majority of patients had improved, and 89% of 55 patients treated only with valvuloplasty were in New York Heart Association functional class I or II. Thus, hemodynamic and clinical improvement can be obtained in the majority of patients with mitral stenosis treated with balloon valvuloplasty in multiple centers. However, suboptimal results and major complications occurred in a significant number of patients and may limit this procedure to use by experienced operators in hospitals with facilities for cardiac surgery.

Volume overload hypertrophy in a closed-chest model of mitral regurgitation.

Chronic volume overload hypertrophy as seen in mitral regurgitation in humans eventually may cause left ventricular dysfunction. Longitudinal study of the mechanisms leading to such dysfunction is difficult in humans and more easily performed in an animal model. In this study, we describe a canine model of volume overload hypertrophy produced by mitral regurgitation. An arterially placed grasping forceps was used to disrupt mitral chordae or leaflets; thus mitral regurgitation was produced without the need for thoracotomy. Eleven of 22 dogs had severe mitral regurgitation (regurgitant fraction greater than 0.50) and survived for greater than or equal to 3 mo (average 9.2 +/- 6 mo) after the production of mitral regurgitation. At 3 mo, end-diastolic volume increased from 48 +/- 9 to 85 +/- 19 ml, P less than 0.01. Left ventricular mass increased from 71 +/- 13 to 90 +/- 10 g, P less than 0.01. Left ventricular end-diastolic pressure increased from 9 +/- 3 to 19 +/- 6 mmHg, P less than 0.01. Cardiac output decreased from 2.3 +/- 0.61 to 1.80 +/- 0.64 l/min, P less than 0.05. The mass-to-volume ratio decreased from 1.44 +/- 0.17 to 1.09 +/- 0.13, P less than 0.01. We conclude that this closed-chest model of chronic mitral regurgitation produces significant eccentric cardiac hypertrophy. Despite a doubling of end-diastolic volume, there was a fall in cardiac output and a rise in left ventricular end-diastolic pressure, suggesting cardiac decompensation.

Sources of subjective variability in the assessment of left ventricular regional wall motion from contrast ventriculograms.

Intraobserver and interobserver variability in the subjective interpretation of angiographic regional wall motion was quantitated in 135 contrast left ventriculograms showing a wide range of normal and abnormal cardiac function, and the effects of rating-scale complexity and myocardial regional differences were examined. Three experienced observers separately graded endocardial motion on a 6-point scale (0 = normal to 5 = dyskinesia) in each of 5 regions. Scores were also tabulated on a 3-point scale and as normal or abnormal. Average intraobserver agreement (2 evaluations per observer) was 68% using the 6-point scale, 86% using the 3-point scale and 90% for normal/abnormal. Interobserver agreement (3 observers) was 47% for exact agreement using the 6-point scale, 75% using the 3-point scale and 80% for normal/abnormal. Interobserver agreement was 84% within a range of 1 wall motion grade on the 6-point scale. Subjectively normal wall motion was most frequent in the 2 basal segments and least frequent in the apical and anterolateral segments. Disagreements were most frequent in the latter 2 segments, but when normal segments were excluded, these interregional differences disappeared. Thus, intraobserver and interobserver agreement is higher than previously reported, and may exceed 80%. Variability depends on whether regional wall motion is normal, but is also affected by the complexity of the rating scale. The distinctions implied by a 6-point subjective rating scale are probably not reliable, but variability is greatly reduced by use of a simplified scoring system.

Aspirin and dipyridamole in the prevention of acute coronary thrombosis complicating coronary angioplasty.

To test the hypothesis that pretreatment with adequate antiplatelet therapy reduces the likelihood of acute coronary thrombosis during routine percutaneous transluminal coronary angioplasty (PTCA), we reviewed, blinded to treatment group, the films and records of 300 consecutive initially successful PTCAs. Films before PTCA, immediately after, and at least 30 min after the last balloon inflation were assessed for the presence of any thrombus at the PTCA site. We excluded 37 patients who received streptokinase before PTCA or who had 100% occlusion or thrombus on pre-PTCA films. New thrombi were classified as clinically significant (defined as causing 100% occlusion or requiring emergency surgery or streptokinase therapy) or as not significant (not causing an acute problem or requiring intervention). Patients were classified into three groups, based on the type and extent of antiplatelet therapy received. Group 1 (no aspirin, n = 121) consisted of patients who did not receive aspirin either before admission or in hospital before PTCA (with or without dipyridamole). Group 2 (standard treatment, n = 110) received aspirin with or without dipyridamole but did not receive both drugs before admission and in hospital before PTCA. Group 3 (maximal treatment, n = 32) received both aspirin and dipyridamole before admission and in hospital before PTCA. New thrombi were detected at 39 (14.8%) PTCA sites, of which 15 (5.7% of all PTCA sites) were considered clinically significant. Group 1 had the highest incidence of both thrombus (21.5%) and clinically significant thrombus (10.7%). A reduction was seen in group 2 in thrombus (11.8%; p = .07) and in clinically significant thrombus (1.8%; p = .005). Group 3 had no thrombus (p = .001) and no clinically significant thrombus (p = .04). In addition to inadequate pretreatment with antiplatelet therapy, univariate analyses demonstrated several other risk factors for thrombus: higher percent diameter stenosis before PTCA (p less than .008), higher platelet count (p = .013), and current smoking (p = .03). Only higher platelet count (p less than .001) and inadequate pretreatment (p = .001) were associated with clinically significant thrombus. Stepwise logistic regression analysis demonstrated that for thrombus, the lack of effective antiplatelet therapy was the most discriminatory variable, followed by current smoking, higher percent diameter stenosis, and dissection. For clinically significant thrombus, once the lack of pretreatment with effective antiplatelet therapy was considered, no other factors added significant discriminatory information.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of exercise and nitroprusside on left ventricular ejection dynamics in idiopathic dilated cardiomyopathy.

To characterize the abnormal pattern of instantaneous left ventricular (LV) ejection in heart failure, proximal aortic pressure, flow, acceleration, power and dW/dt were measured at rest and during supine bicycle exercise using high-fidelity, catheter-mounted pressure and velocity sensors in 16 patients with idiopathic dilated cardiomyopathy (IDC) and 11 normal control subjects. In patients with IDC, peak flow was lower than normal both at rest (454 +/- 155 vs 649 +/- 168 ml/s, p less than 0.01) and during exercise (569 +/- 213 vs 916 +/- 329 ml/s, p less than 0.01). Peak acceleration, power and dW/dt were also significantly reduced in patients with IDC at rest and during exercise. Time to peak flow (as a fraction of LV ejection time) was consistently prolonged in patients with IDC (rest, 0.40 +/- 0.08 vs 0.29 +/- 0.04; exercise, 0.36 +/- 0.06 vs 0.28 +/- 0.04, both p less than 0.01). Exercise-induced increments in peak flow, power and dW/dt were significantly blunted in patients with IDC. Studies during pacing tachycardia and nitroprusside administration failed to reproduce the abnormalities during exercise in patients with IDC. Thus, the instantaneous flow pulse in heart failure is both diminished in magnitude (decreased stroke volume and peak flow) and abnormal in shape (decrease peak acceleration and delayed time to peak flow). Exercise stress in IDC results in abnormalities of LV performance that can be detected using instantaneous ejection information. These abnormalities are unlikely to be explained by changes in heart rate or loading conditions.

Effects of six-month afterload reduction therapy with hydralazine in chronic aortic regurgitation.

Seventeen patients with chronic asymptomatic aortic regurgitation (AR) were studied to determine whether 6 months of hydralazine therapy can reduce the severity of AR or reverse left ventricular (LV) enlargement and hypertrophy. Echocardiography, radionuclide angiography at rest and during exercise, and maximal treadmill exercise with respiratory gas analysis were performed at intake and after a 6-month double-blind treatment period. After dose titration with hydralazine, patients were randomized to their maximal tolerated hydralazine dose or to placebo. At intake, hydralazine and placebo groups were similar. Six patients taking hydralazine and 8 taking placebo completed the study protocol. One patient taking placebo died and 2 patients taking hydralazine withdrew with drug-related adverse effects. The mean titrated dose of hydralazine was 96 +/- 9 mg, but the mean treatment dose was 63 +/- 21 mg administered 3 times daily because of drug intolerance. After 6 months, mean systolic blood pressure with hydralazine therapy decreased from 136 to 125 mm Hg (p less than 0.02), and end-systolic posterior wall thickness increased from 1.58 to 1.70 cm (p less than 0.05), resulting in a significant reduction in M-mode meridional end-systolic stress (from 104 to 80 kdynes/cm2) (p less than 0.05). M-mode fractional shortening increased from 0.28 to 0.31 (p less than 0.05) with hydralazine, but mean LV echocardiographic dimensions were unchanged. LV mass increased from 383 to 434 g (p less than 0.05) with hydralazine primarily because of an increase in end-diastolic wall thickness. In the placebo group, there was no change in any of the hemodynamic or echocardiographic parameters at 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Characteristics of vascular hydraulic load in patients with heart failure.

Aortic input impedance and hydraulic power were derived from simultaneous catheter recordings of ascending aortic pressure and velocity in eight normal subjects and 11 age-matched subjects with clinical heart failure secondary to idiopathic congestive cardiomyopathy. Resting data revealed the characteristic depression of cardiac output and elevation of systemic vascular resistance in patients with heart failure. The pulsatile component of vascular hydraulic load, characteristic impedance (Zc), was similar in both groups (Zc normal: 85 +/- 30 dyne-sec-cm-5; Zc cardiomyopathy: 93 +/- 33 dyne-sec-cm-5). The oscillatory fraction of aortic input power in patients with heart failure (14 +/- 4%) was also similar to that of normal subjects (11 +/- 2%). The transition from rest to exercise in patients with heart failure was marked by a decrease in the steady component of arterial hydraulic load, although characteristic impedance did not change. A similar qualitative response occurred in normal subjects, although the systemic vascular resistance during exercise remained above normal in patients with heart failure. The modulus of the first harmonic of impedance significantly decreased during exercise in normal subjects but did not change significantly in patients with heart failure. Furthermore, the modulus of the first harmonic of the reflection coefficient decreased significantly during exercise in normal subjects but did not change in patients with heart failure in spite of systemic vasodilation. Exercise appears to impose no additional increase in vascular hydraulic load on the ejecting left ventricle. The similar aortic characteristic impedances in patients with heart failure and in normal subjects, at rest and during exercise, are consistent with a constant oscillatory fraction of input power.

Acute coronary vasoconstrictive effects of cigarette smoking in coronary heart disease.

To investigate the effect of cigarette smoking on the coronary vasculature, coronary sinus flow and myocardial oxygen delivery were measured at rest and during incremental atrial pacing in 10 patients with coronary artery disease. Measurements were then repeated while the patients smoked 2 unfiltered, high-nicotine cigarettes. Although smoking significantly increased the heart rate at rest and double product, coronary sinus flow did not change significantly (141 +/- 32 vs 146 +/- 28 ml/min). At the lowest equivalent pacing rate before and during smoking, the double products were comparable. However, coronary sinus flow was reduced by smoking (146 +/- 28 vs 159 +/- 28 ml/min, p less than 0.01) and coronary vascular resistance was increased (0.96 +/- 0.15 vs 0.83 +/- 0.13 mm Hg ml-1 min, p less than 0.02). The double products were also comparable at the peak pacing rate before and during smoking. Nonetheless, the coronary sinus flow was again lower (167 +/- 23 vs 227 +/- 41 ml/min, p = 0.02) and the coronary vascular resistance was higher (0.77 +/- 0.10 vs 0.63 +/- 0.09 mm Hg ml-1 min, p less than 0.01) during smoking. The transmyocardial arteriovenous oxygen difference was unchanged by smoking; therefore, myocardial oxygen delivery was reduced in proportion to the reductions in coronary sinus flow. Thus, cigarette smoking appears to acutely alter the ability of the coronary vasculature to regulate flow in accordance with the oxygen requirements of the myocardium.

Validation of Fourier amplitude ratio to quantitate valvular regurgitation.

It has previously been shown that patients with valvular regurgitation can be identified by the ratio of left and right ventricular amplitude values obtained from first harmonic Fourier analysis of the gated blood pool scan. The present study was designed to validate the accuracy of this technique for quantifying the amount of valvular regurgitation. In a blinded analysis of 19 patients who underwent cardiac catheterization, there was a close correlation between the radionuclide and hemodynamic determination of the amount of regurgitation (r = 0.84). The interobserver agreement for calculating the radionuclide data was also high (r = 0.88). These results suggest that the Fourier ventricular amplitude ratio is an accurate and reproducible technique for quantifying valvular regurgitation by gated blood pool scanning.