PubMed Health⌕ Search

Biomedical subjects

D R Rosing

Publications and source records attributed to D R Rosing.

At least 37 records · Page 2Linked to original sources
PubMed1985

Dynamic subaortic obstruction in hypertrophic cardiomyopathy: analysis by pulsed Doppler echocardiography.

To determine whether true obstruction to left ventricular ejection exists in patients with hypertrophic cardiomyopathy and a subaortic gradient, pulsed Doppler echocardiography was used to analyze the patterns of left ventricular emptying in 50 patients with hypertrophic cardiomyopathy (20 with and 30 without evidence of obstruction) and in 20 normal subjects. In obstructive hypertrophic cardiomyopathy, left ventricular ejection was characterized by early and rapid emptying (76 +/- 14% of aortic flow velocity in the initial one-third of systole). The proportion of forward flow velocity occurring before initial mitral-septal contact (and hence, by inference before the onset of the subaortic gradient) was variable, but averaged 58%. In contrast, the proportion of forward flow velocity occurring after mitral-septal contact (and, therefore, concomitant with the gradient and increased intraventricular pressure) was considerable, averaging over 40%. Mid-systolic impedance to left ventricular outflow was suggested by the rapid deceleration in aortic flow velocity concomitant with mitral-septal contact and premature partial aortic valve closure. Furthermore, left ventricular ejection was prolonged (384 +/- 40 ms) and the ventricle continued to empty and shorten during the period when both the pressure gradient and markedly increased intraventricular pressures were present. In 16 of 20 patients, a relatively small second peak in flow velocity appeared in late systole. Since marked systolic anterior motion of the mitral valve was still present, the late systolic portion of forward flow velocity also appeared to be largely ejected during imposition of a mechanical impediment to outflow. In contrast, patients with nonobstructive hypertrophic cardiomyopathy showed no evidence of impedance to left ventricular ejection. Aortic flow velocity waveforms were similar to those of normal subjects, with flow persisting to aortic valve closure; significant mitral systolic anterior motion and partial mid-systolic aortic valve closure were absent, and the systolic ejection period was normal (303 +/- 27 ms).(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1985

Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve.

Thirty-three patients with chest pain despite angiographically normal coronary arteries underwent both coronary flow studies during pacing and resting and exercise gated blood pool scintigraphy. During atrial pacing after administration of ergonovine, those patients developing their typical chest pain demonstrated significantly lower great cardiac vein flow (97 +/- 31 vs 150 +/- 33 ml/min, p less than .001), higher coronary resistance (1.27 +/- 0.43 vs 0.77 +/- 0.18 mm Hg/ml/min, p less than .005), and less lactate consumption (30.5 +/- 22.0 vs 69.7 +/- 41.1 mM . ml/min, p less than .005) and a higher left ventricular end-diastolic pressure after pacing (20 +/- 4 vs 12 +/- 1, p less than .001) compared with those without pain and in the absence of significant luminal narrowing of the epicardial coronary arteries. The 26 patients with abnormal vasodilator reserve demonstrated reduced left ventricular ejection fraction during exercise (58 +/- 8%) compared with the seven patients with appropriate vasodilator reserve (66 +/- 4%, p less than .05) and with a group of 52 control patients of similar age and sex distribution and free of known heart disease (66 +/- 10%, p less than .001). In addition, 12 of the 26 patients with abnormal vasodilator reserve demonstrated exercise-induced regional wall motion abnormalities. Many of these patients also manifested impaired left ventricular diastolic filling at rest compared with the control subjects (peak filling rate 2.6 +/- 0.7 vs 3.2 +/- 0.7 end-diastolic volume/sec, p less than .005). Thus, patients with chest pain resulting from abnormal vasodilator reserve demonstrate abnormalities of left ventricular systolic and diastolic function suggestive of myocardial ischemia.

Adult↗
PubMed1985

Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures.

To study the mechanism and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 20 patients (nine with resting left ventricular outflow tract obstruction greater than or equal to 30 mm Hg) with a history of angina pectoris and angiographically normal coronary arteries underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared with 28 control subjects without hypertrophic cardiomyopathy, their resting coronary blood flow was higher (91 +/- 27 vs 66 +/- 17 ml/min; p less than .001) and their coronary resistance was lower (1.13 +/- 0.38 vs 1.55 +/- 0.45 mm Hg/ml/min; p less than .001). Left ventricular end-diastolic pressure (16 +/- 6 vs 11 +/- 3 mm Hg; p less than .001) and pulmonary arterial wedge pressure (13 +/- 5 vs 7 +/- 3 mm Hg; p less than .001) were significantly higher in patients with hypertrophic cardiomyopathy. During pacing, coronary flow rose in both groups, although coronary and myocardial hemodynamics differed greatly. In contrast to the linear increase in flow in control subjects up to heart rate of 150 beats/min (66 +/- 17 to 125 +/- 28 ml/min), patients with hypertrophic cardiomyopathy demonstrated an initial rise in flow to 133 +/- 31 ml/min at an intermediate heart rate of 130 beats/min. At this point, 12 of 20 patients developed their typical chest pain. With continued pacing to a heart rate of 150 beats/min, mean coronary flow fell to 114 +/- 29 ml/min (p less than .002), with 18 of 20 patients experiencing their typical chest pain and metabolic evidence of myocardial ischemia. This fall in coronary flow was associated with a substantial rise in left ventricular end-diastolic pressure (30 +/- 9 mm Hg immediately after peak pacing). In the 14 patients whose coronary flow actually fell from intermediate to peak pacing, the rise in left ventricular end-diastolic pressure in the same interval was greater than that of the six patients whose flow remained unchanged or increased (11 +/- 8 vs 2 +/- 2 mm Hg; p less than .01). In addition, despite metabolic and hemodynamic evidence of myocardial ischemia, the arteriovenous O2 difference actually narrowed at peak pacing. Thus most patients with hypertrophic cardiomyopathy achieved maximum coronary vasodilation and flow at modest increases in heart rate. Elevation in left ventricular filling pressure, probably related to ischemia-induced changes in ventricular compliance, was associated with a decline in coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects.

Verapamil improves exercise tolerance and decreases symptoms in many patients with hypertrophic cardiomyopathy. The mechanisms responsible for these effects are not completely understood, although previous studies indicate that verapamil enhances left ventricular relaxation and diastolic filling in such patients. To investigate the association between changes in left ventricular filling and exercise tolerance after verapamil, we studied 55 patients with hypertrophic cardiomyopathy by radionuclide angiography and graded treadmill testing before and after 1 to 4 weeks of therapy with orally administered verapamil, 320 to 640 mg/d. The verapamil-induced increase in peak left ventricular filling rate at rest (from 3.1 +/- 1.3 to 3.7 +/- 1.3 end-diastolic volumes/sec; p less than .001) was associated with an increase in exercise tolerance (from 5.9 +/- 3.6 to 8.7 +/- 4.7 min; p less than .001); exercise capacity increased in 34 of 43 patients (79%) manifesting an increase in peak filling rate but only one of 12 patients (8%) with unchanged or decreased peak filling rate (p less than .001). This initial trend persisted in 25 patients studied after 1 year of therapy; 11 of 16 patients (69%) with a persistent increase in peak filling rate had persistent improvement in exercise tolerance relative to preverapamil values, compared with only one of nine patients (11%) in whom peak filling rate was unchanged or decreased relative to preverapamil levels (p less than .02). Verapamil withdrawal after 1 to 2 years in 24 patients resulted in reduction in peak filling rate (p less than .001) and was associated with deterioration in exercise tolerance in 17 patients (71%). Hence, verapamil-induced changes in left ventricular peak filling rate were associated significantly with objective symptomatic improvement. These data support the concept that enhanced left ventricular diastolic filling is an important mechanism contributing to the clinical improvement experienced by many patients with hypertrophic cardiomyopathy during therapy with verapamil.

Adolescent↗
PubMed1985

Effects of sublingual nifedipine on hemodynamics and systolic and diastolic function in patients with hypertrophic cardiomyopathy.

The hemodynamic effects of sublingual nifedipine were examined in 36 patients with hypertrophic cardiomyopathy. Twenty-one patients were initially given 20 mg and 15 patients were given 10 mg of the drug; 30 min after this first dose 26 patients received 10 mg and one patient 20 mg as a second dose. Hemodynamic findings in patients who received different doses of the drug were similar. Peak effects included an increase in heart rate from 79 +/- 12 to 91 +/- 14 (mean +/- 1 SD) beats/min (p less than .01), and a decrease in mean blood pressure from 89 +/- 12 to 77 +/- 10 mm Hg (p less than .01). Cardiac index increased after nifedipine (2.8 +/- 0.6 to 3.3 +/- 0.8 liters/min/m2; p less than .01); stroke volume index, however, did not change (36 +/- 7 to 36 +/- 8 ml/beat/m2; NS). Peripheral vascular resistance index fell significantly from 822 +/- 261 to 610 +/- 197 dynes X sec X cm-5 (p less than .01). Overall, left ventricular outflow tract gradient (LVOTG) did not change in patients with significant (greater than or equal to 30 mm Hg) basal LVOTG (75 +/- 22 to 83 +/- 22 mm Hg; NS), but it increased significantly in those six patients in whom peripheral vascular resistance fell by 25% or more (73 +/- 28 to 99 +/- 22 mm Hg; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Survival and functional results after valve replacement for aortic regurgitation from 1976 to 1983: impact of preoperative left ventricular function.

Recent studies suggest that preoperative left ventricular function may no longer be an important determinant of survival or functional results after operation for aortic regurgitation because of improved operative techniques. To assess the effect of left ventricular function on prognosis in the current surgical era, we performed echocardiographic and radionuclide angiographic studies in 80 consecutive patients undergoing valve replacement from 1976 to 1983. No patient had associated coronary artery disease. For all patients, 5 year survival was 83 +/- 5%, significantly better than the 62 +/- 9% 5 year survival in our patients operated on from 1972 to 1976. Preoperative resting left ventricular ejection fraction (p less than .001), fractional shortening (p less than .001), and end-systolic dimension (p less than .01) were the most significant predictors of survival (univariate life-table analysis). Five year survival was 63 +/- 12% in patients with subnormal ejection fraction (n = 50) compared with 96 +/- 3% in those with normal ejection fraction (n = 30). Patients with subnormal left ventricular ejection fraction and poor exercise tolerance or prolonged duration of left ventricular dysfunction (greater than 18 months) comprised the high-risk subgroup (5 year survival 52 +/- 11%). Patients in this subgroup also had persistent left ventricular dysfunction after operation, with greater left ventricular end-diastolic dimensions and reduced ejection fraction (both p less than .001) compared with patients with normal preoperative left ventricular ejection fraction or a brief duration of left ventricular dysfunction (less than 14 months). Cold hyperkalemic cardioplegia was used for myocardial preservation in 46 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1985

Evaluation of myocardial function by invasive methods.

The evaluation of myocardial performance requires an understanding of the contributions of loading conditions (preload and afterload), heart rate, and contractility. Although the measurement of these parameters often requires specialized techniques, more easily performed invasive evaluation can take place applying the principles derived from an understanding of the factors affecting cardiac performance. The construction of ventricular function curves permits the evaluation of the influence of preload on the work of the heart. Changes in afterload and/or myocardial contractility can produce a series of such function curves. Construction of pressure-volume loops and the examination of end-systolic pressure-volume relationships offer insights into the status of myocardial contractility apart from loading conditions, as well as into the response of the heart to acute and chronic alteration in loading conditions. Ventricular function curves can be obtained during exercise, pacing, and pharmacologic intervention in order to detect subtle cardiac dysfunction, to assess the severity of dysfunction, and to gauge the response to therapy.

Angiography↗
PubMed1984

Exercise-induced ischemia in mildly symptomatic patients with coronary-artery disease and preserved left ventricular function. Identification of subgroups at risk of death during medical therapy.

To determine prospectively whether the severity of reversible left ventricular ischemia provides prognostic information in mildly symptomatic patients with coronary-artery disease and preserved left ventricular function at rest (ejection fraction greater than 40 per cent), we studied 117 patients by means of exercise electrocardiography and radionuclide angiography. No patient had stenosis of the left main coronary artery. Mortality during subsequent medical therapy was significantly associated (by univariate life-table analysis) with three-vessel coronary-artery disease and the magnitude of the ejection fraction during exercise. In patients with three-vessel disease who had both ST-segment depression of 1 mm or more and a decrease in ejection fraction during exercise, in association with an exercise tolerance of 120 W or less, the probability of survival at four years was only 71 +/- 11 per cent (S.E.). All deaths occurred in this subgroup. Thus, objective evidence of left ventricular ischemia during exercise and exercise capacity identify one subgroup of minimally symptomatic patients with three-vessel disease with an excellent prognosis and another subgroup at relatively high risk of dying during subsequent medical therapy.

Adult↗
PubMed1984

Exercise, electrocardiographic and functional responses after percutaneous transluminal coronary angioplasty.

Exercise testing after successful PTCA showed improved cardiac functional status on examination of electrocardiographic and symptomatic responses, myocardial perfusion and global and regional left ventricular function. Sixty-six patients were studied before and after persistently successful PTCA. Follow-up studies an average of 8 months after the successful procedure showed an incidence of abnormal testing of only 7% using both electrocardiographic and subjective symptomatic criteria during treadmill studies and no abnormal studies with thallium scintigraphy. Radionuclide cineangiography demonstrated similar left ventricular ejection fractions at rest before and after PTCA, but an improvement of 9 +/- 10% (p less than 0.001) in the exercise ejection fraction at follow-up. However, 52% of patients with paired data still had an abnormal radionuclide cineangiographic study after successful PTCA, raising the question of the presence of subclinical ischemia or a false-positive result.

Angioplasty, Balloon↗
PubMed1984

Reversal of left ventricular dysfunction after aortic valve replacement for chronic aortic regurgitation: influence of duration of preoperative left ventricular dysfunction.

Preoperative left ventricular systolic function is an important predictor of postoperative prognosis in patients with aortic regurgitation. Although left ventricular dysfunction is reversible after aortic valve replacement to a greater extent in patients with good preoperative exercise capacity compared with patients with impaired exercise capacity, not all patients with preserved exercise capacity demonstrate improved left ventricular function after aortic valve replacement. To determine the influence of duration of preoperative left ventricular dysfunction on postoperative reversal of left ventricular dysfunction, we studied 37 patients with aortic regurgitation who preoperatively had left ventricular dysfunction, defined as subnormal echocardiographic fractional shortening (less than 29%), and good preoperative exercise capacity, defined as completion of stage I of the NIH treadmill protocol without limiting symptoms. Eight patients were asymptomatic. In 11 patients left ventricular dysfunction was documented 18 to 57 months preoperatively (prolonged); in 10 patients left ventricular dysfunction developed in an interval of 14 months or less preoperatively (brief); in 16 patients duration of left ventricular dysfunction was unknown. Patients with brief vs those with prolonged left ventricular dysfunction did not differ with respect to severity of preoperative symptoms or exercise tolerance, echocardiographically determined left ventricular dimensions or fractional shortening (25 +/- 3% [SD] vs 25 +/- 3%), or radionuclide angiographic ejection fraction (42 +/- 5% vs 42 +/- 5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Morphologic determinants of hemodynamic state after ventricular septal myotomy-myectomy in patients with obstructive hypertrophic cardiomyopathy: M mode and two-dimensional echocardiographic assessment.

To define the morphologic features of the left ventricle after ventricular septal myotomy-myectomy and to elucidate the structural changes associated with a postoperative reduction in the pressure gradient, 28 patients with obstructive hypertrophic cardiomyopathy were studied with M mode and qualitative and quantitative two-dimensional echocardiography. Nine patients with a marked reduction in the pressure gradient (no or small, less than or equal to 25 mm Hg, residual basal gradient) demonstrated a marked reduction in septal thickness after surgery (23 +/- 6 to 13 +/- 4 mm; p less than .01), a concomitant increase in septal to mitral valve distance (20 +/- 2 to 30 +/- 5 mm; p less than .005), and a loss or substantial decrease in the magnitude of systolic anterior motion of the mitral valve. Two-dimensional echocardiographic results demonstrated an increase of over 100% in the cross-sectional area of the left ventricular outflow tract at onset of systole (2.2 +/- 0.6 to 5.5 +/- 3 cm2; p less than .01). In six of the patients postoperative paradoxic septal motion appeared to contribute importantly to the increased size of the outflow tract during ventricular systole. In contrast, nine patients with little or no change in the pressure gradient (residual basal gradient greater than or equal to 40 mm Hg) demonstrated a less marked decrease in septal thickness and no significant change in septal to mitral valve distance or magnitude of mitral systolic anterior motion. Furthermore, the postoperative left ventricular outflow tract area was significantly smaller in patients with residual basal gradients (3.0 +/- 1 cm2) than that in patients with no residual gradient (5.5 +/- 3 cm2; p less than .05). Ten patients with only provocable subaortic gradients after operation showed postoperative left ventricular outflow tract dimensions intermediate between those in patients with either residual basal gradient or no residual gradient. On the basis of this echocardiographic assessment of septal myotomy-myectomy, we conclude that abolition or reduction of the subaortic gradient after operation in patients with obstructive hypertrophic cardiomyopathy is largely the consequence of surgical enlargement of the left ventricular outflow tract area.

Adolescent↗
PubMed1983

Atrial systole and left ventricular filling in hypertrophic cardiomyopathy: effect of verapamil.

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.

Adult↗
PubMed1983

The acute and chronic effects of verapamil on left ventricular function in patients with hypertrophic cardiomyopathy.

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.

Blood Pressure↗
PubMed1983

Effects of verapamil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy: pressure-volume analysis with a nonimaging scintillation probe.

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.

Adult↗
PubMed1983

Nonsurgical myocardial revascularization: initial experience with percutaneous transluminal coronary angioplasty.

Coronary artery atheromata obstruct coronary blood flow and produce myocardial ischemia. Percutaneous transluminal coronary angioplasty (PTCA) was performed to dilate narrowed coronary arteries on 16 occasions in 15 patients with severe proximal coronary artery narrowings and significant clinical angina pectoris. The lesions involved the left-anterior descending (LAD) coronary artery in nine patients (10 dilatation procedures), the right coronary artery (RCA) in five, and the circumflex coronary artery in one. Successful dilatation was achieved on nine occasions (56%): in 7 of the 10 LAD lesions (70%), in 2 of the 5 RCA lesions (40%), but not in the patient with circumflex disease. Successful dilatation was accompanied by a significant improvement in symptoms and in myocardial performance, as judged by atrial pacing MUGA (multigated) ventriculography. The ischemic response of the ventricle to stress the significantly reduced or abolished. PTCA is a useful, nonoperative method for dilating obstructed coronary arteries and for improving myocardial blood flow.

Adult↗
PubMed1982

Improved myocardial function during exercise after successful percutaneous transluminal coronary angioplasty.

Fifty-nine consecutive patients with coronary-artery disease undergoing percutaneous transluminal coronary angioplasty were evaluated with radionuclide ventriculography at rest and during exercise before angioplasty (when possible) and afterward when it was successful. Thirty-eight patients (64 per cent) had an angiographically successful procedure. Three (5 per cent) had coronary occlusion as a complication. Arterial stenosis was reduced from 74 +/- 2 per cent to 31 +/- 3 per cent (mean +/- S.E.M.). The mean ejection fraction was 55 +/- 2 per cent at rest and 51 +/- 3 per cent during exercise before the procedure. After successful angioplasty, the ejection fraction was unchanged at rest but increased to 62 +/- 2 per cent (P less than 0.001) during exercise. Regional dysfunction was present during exercise in 94 per cent of the patients before the procedure and in only 8 per cent after successful angioplasty. Of the 38 patients in whom the procedure was successful, 19 had sustained improvement for over six months, and eight for three to six months. Eleven patients had recurrence of symptoms; the second angioplasty was initially successful in nine. In 24 patients remaining asymptomatic for six months (19 after the first procedure and five after the second), the left ventricular ejection fraction during exercise remained stable or improved.

Adult↗