Improved left ventricular diastolic filling in patients with coronary artery disease after percutaneous transluminal coronary angioplasty

Left ventricular (LV) diastolic filling is abnormal at rest in many patients with coronary artery disease (CAD), even in the presence of normal resting LV systolic function. To determine the effects of improved myocardial perfusion on impaired. LV diastolic filling, we studied 25 patients with one-vessel CAD by high-temporal-resolution radionuclide angiography before and after percutaneous transluminal coronary angioplasty (PTCA). No patient had ECG evidence of previous myocardial infarction. Despite normal regional and global LV systolic function at rest in all patents, LV diastolic filling was abnormal (peak LV filling rate [PFR] less than 2.5 end-diastolic volumes (EDV)/sec or time to PFR greater than 180 msec) in 17 of 25 patients. Twenty-three patients had abnormal LV systolic function during exercise. After successful PTCA, LV ejection fraction and heart rate at rest were unchanged, but LV ejection fraction during exercise increased, from 52 +/- 8% (+/- SD) to 63 +/- 5% (p less than 0.001). LV diastolic filling at rest improved: PFR increased from 2.3 +/- 0.6 to 2.8 +/- 0.5 EDV/sec (p less than 0.001) and time to PFR decreased from 181 +/- 22 to 160 +/- 18 msec (p less than 0.001). Thus, a reduction in exercise-induced LV systolic dysfunction after PTCA, reflecting a reduction in reversible ischemia, was associated with improved LV diastolic filling at rest. These data suggest that in many CAD patients with normal resting LV systolic function and without previous infarction, abnormalities of resting LV diastolic filling are not fixed, but appear to be reversible manifestations of impaired coronary flow.     

Left and right ventricular function during symptom-limited exercise in patients with isolated mitral stenosis

Ventricular function during exercise in patients with mitral stenosis has not been widely studied. Accordingly, 20 patients with isolated mitral stenosis were assessed during supine, symptom-limited equilibrium radionuclide ventriculographic studies. All patients had a normal left ventricular (LV) ejection fraction at rest (greater than or equal to 50 percent), and all were in sinus rhythm. Left ventricular ejection fraction rose (p less than 0.001) from 64 +/- 9 percent at rest to 74 +/- 11 percent during exercise. This normal response was due solely to a decrease (p less than 0.01) in exercise LV end-systolic volume. A significant (p less than 0.01) decrease in end-diastolic volume during exercise limited the increase in ejection fraction during exercise. The decrease in end-diastolic volume during exercise caused stroke volume to remain unchanged; cardiac output rose according to heart rate alone. Right ventricular (RV) ejection fraction did not rise with exercise due to an increase in end-systolic volume. With exercise, LV end-diastolic volume was smaller (p less than 0.05) with severe mitral stenosis compared to mild mitral stenosis. With exercise, RV ejection fraction was decreased (p less than 0.05) with severe compared to mild mitral stenosis. In conclusion, LV function during exercise is normal in patients with normal resting LV ejection fraction. A decrease in LV diastolic filling with exercise prevents a rise in stroke volume, and cardiac output increases by heart rate alone. With, exercise, RV ejection fraction does not rise, due to an increase in RV end-systolic volume.     

Percutaneous transluminal coronary angioplasty: determination of left ventricular function in physical stress using intravenous digital subtraction angiocardiography

24 patients with coronary artery disease underwent intravenous digital subtraction angiocardiography at rest and during exercise before and after percutaneous transluminal coronary angioplasty (PTCA). Before PTCA mean pulmonary artery pressure increased pathologically in 20 patients (on average from 22 +/- 4 to 40 +/- 9 mm Hg, p less than 0.001). The increase in cardiac index from 4.2 +/- 1.3 to 6.2 +/- 2.01 I X min-1 X m-2 (p less than 0.01) was achieved by an increase in heart rate from 77 +/- 13 to 119 +/- 16 min-1 (p less than 0.001) as stroke volume remained unchanged during exercise (52 +/- 14 ml X m-2, resting value: 53 +/- 13 ml X m-2). Though end-systolic volume increased from 32 +/- 11 to 41 +/- 13 ml X m-2 (p less than 0.001) and ejection fraction fell from 63 +/- 8% to 56 +/- 10% (p less than 0.005), stroke volume remained unchanged due to an enhanced diastolic filling (EDVI: 86 +/- 19 ml X m-2 at rest, 92 +/- 18 ml X m-2 during exercise, p less than 0.001). After angiographically successful PTCA in 21 of 24 patients average mean pulmonary artery pressure during exercise remained pathologically elevated (36 +/- 9 mm Hg, no significant difference from value before PTCA). It normalized in only 6 of 17 patients. On the other hand there was a marked improvement of left ventricular systolic performance. Ejection fraction during exercise (65 +/- 11%) was higher than before PTCA (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular ejection dynamics in hypertrophic cardiomyopathy and aortic stenosis: comparison with the use of Doppler echocardiography

Left ventricular ejection dynamics of 15 patients with hypertrophic cardiomyopathy (nine obstructive, six nonobstructive) were compared to those in 12 age-matched normal subjects and 10 patients with valvular aortic stenosis by means of combined two-dimensional and Doppler echocardiography. Doppler peak flow velocities in obstructive (HOCM, 2.5 +/- 1.3 m/sec) and nonobstructive (HNCM, 2.6 +/- 0.6 m/sec) hypertrophic cardiomyopathy, as well as in patients with aortic stenosis (AS, 3.6 +/- 1.3 m/sec) were significantly higher than in the normal population (1.0 +/- 0.2 m/sec; p less than 0.001 for all comparisons), but did not differ from each other. The HOCM patients had time to peak velocity (154 +/- 55.7 msec) that was higher than that in both HNCM (86 +/- 8.4 msec) and normal groups (84.5 +/- 8.9 msec; p less than 0.001 for both comparisons), but did not differ from those in AS (117 +/- 52.5 msec). The total ejection time did not differ between HOCM (348.2 +/- 91.1 msec) and AS (328.8 +/- 30.4 msec) groups, but was prolonged in HOCM compared to HNCM (198 +/- 21.0 msec) and normal groups (233 +/- 28.3 msec; p less than 0.001 for both comparisons). The normal and HNCM groups did not differ in time to peak or total ejection time measurements. The percent of flow velocity present in the initial third of the systolic velocity integral for HOCM (44.5% +/- 5.9) and HNCM (49.4% +/- 2.5) groups was greater than for normals (36.2% +/- 5.4; p less than 0.05 for both comparisons), but HOCM values did not differ from HNCM values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute haemodynamic effects of dopexamine in patients with coronary arterial disease

We assessed the acute haemodynamic effects of dopexamine 1 microgram/kg/min and 3 micrograms/kg/min in 21 patients with coronary arterial disease following routine catheterisation. Patients were aged 38 to 72 years and left ventricular ejection fraction ranged from 23 to 79%. Dopexamine was well tolerated in all patients except one in whom transient ventricular arrhythmias occurred with 3 micrograms/kg/min. No patient developed angina. Dopexamine increased cardiac index (2.6 +/- 0.4 to 3.2 +/- 0.1 (P less than 0.001) and 4.0 +/- 1.0 1/min/m2 (P less than 0.001), control to 1 microgram/kg/min and 3 micrograms/kg/min, respectively) and decreased systemic vascular resistance index (3356 +/- 1506 to 2318 +/- 809 (P less than 0.001) and 2252 +/- 1973 dyne.sec.cm-5/m2 (P less than 0.001], but did not affect systemic arterial, pulmonary arterial or right atrial pressure. Maximum positive dP/dt was increased (1294 +/- 324 to 1597 +/- 505 (P less than 0.001) and 2199 +/- 819 mmHg/sec (P less than 0.001] as was left ventricular stroke work index (44 +/- 20 to 51 +/- 21 (P less than 0.05) and 56 +/- 27 g.m/m2 (P less than 0.001) control to 1 microgram/kg/min and 3 micrograms/kg/min, respectively). Left ventricular end diastolic pressure fell with 3 micrograms/kg/min from 19.8 +/- 6.9 to 12.4 +/- 4.6 mmHg (P less than 0.05) in patients with preserved left ventricular ejection fraction (greater than 50%, n = 6), but not in those with impaired left ventricular ejection fraction (less than 50%, n = 15), otherwise the effects in these two subgroups were similar. We conclude that dopexamine has both inotropic and vasodilator properties.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of bypass operation and balloon angioplasty on heart function at rest]

Improvement of exercise left-ventricular ejection fraction after successful aortocoronary bypass operation and transluminal coronary angioplasty has been demonstrated. The purpose of this study was to investigate in which patients improvement of left-ventricular function at rest can be observed. Radionuclide ventriculography and exercise stress test was carried out in 34 patients before and after successful aortocoronary bypass operation (Group 1), and in 69 patients before and after successful transluminal coronary angioplasty (Group 2). After bypass surgery, mean ejection fraction at rest increased from 42 +/- 11 to 49 +/- 13% (p less than 0.001). Marked improvement (greater than or equal to 5%) was observed in 19 patients (56%) in whom severe myocardial ischemia could be documented during exercise ECG (Group 1.1: Increase of ejection fraction from 40 +/- 14 to 54 +/- 12%, p less than 0.001; ischemia score during exercise test 8.8 +/- 10). In the remaining 15 patients no significant improvement occurred (Group 1.2: 43 +/- 16 vs. 43 +/- 16%, p = n.s.; ischemia score during exercise test 3.2 +/- 2.4, p = 0.02 vs. Group 1.1). After angioplasty, resting left-ventricular ejection fraction increased, on average, from 50 +/- 11 to 52 +/- 12% (p less than 0.001). Comparable to the results observed in patients after surgery, improvement was most pronounced in patients with severe exercise-induced ST-depression (Group 2.1: Increase of ejection fraction from 49 +/- 10 to 58 +/- 10%, p less than 0.001; ischemia score during exercise 2.5 +/- 2.3).(ABSTRACT TRUNCATED AT 250 WORDS)     

The acute effects of intravenous xamoterol ('Corwin', I.C.I. 118, 587) on resting and exercise haemodynamics in patients with mild to moderate heart failure

The known properties of xamoterol, a partial beta 1-agonist, provide a basis to pharmacologically modulate cardiac responses to variations in sympathetic tone. Haemodynamic variables were assessed at rest and on exercise before and after intravenous xamoterol (0.2 mg kg-1), in 30 patients with mild to moderate cardiac failure. Xamoterol produced significant improvements in resting cardiac index (2.51 +/- 0.15 to 2.80 +/- 0.14 l min-1 m-2; P less than 0.001), stroke volume (62 +/- 4 to 75 +/- 5 mljbeat-1; P less than 0.001) and stroke work index (42.4 +/- 3.6 to 47.7 +/- 3.9 gm beat-1 m-2; P less than 0.01). This occurred despite a significant reduction in heart rate (78 +/- 3 to 74 +/- 2 beats min-1; P less than 0.05). There were also significant reductions in systemic vascular resistance (1990 +/- 141 to 1669 +/- 112 dynes s-1 cm-5; P less than 0.01) and double product (1146 +/- 46 to 1051 +/- 41 mmHg min-1 x 10(-1); P less than 0.05), with no significant changes in systolic blood pressure, pulmonary wedge pressure or ejection fraction. Xamoterol significantly attenuated the heart rate response to exercise (112 +/- 4 to 97 +/- 3 beats min-1; P less than 0.001), with no impairment in the expected exercise induced increase in cardiac index. This was due to the significant increase in stroke volume from 81 +/- 6 to 95 +/- 7 ml beat-1 (P less than 0.001). There were no significant changes in resting or exercise noradrenaline levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamically important right ventricular infarction: follow-up evaluation of right ventricular systolic function at rest and during exercise with radionuclide ventriculography and respiratory gas exchange

The prognosis and recovery of right ventricular systolic function in patients with hemodynamically documented right ventricular myocardial infarction (RVMI) is unclear. Therefore 27 patients who met hemodynamic criteria for RVMI were followed for at least 1 year. Four patients died within 1 year and 23 survived. Postmortem examination performed in three of the four patients showed extensive infarction of the right and left ventricles. Survivors underwent early and late follow-up resting radionuclide ventriculograms and late exercise studies. During long-term follow-up (1 to 4 years) resting radionuclide ventriculography demonstrated a significant improvement in right ventricular ejection fraction (30 +/- 7% to 43 +/- 8%; p less than .001) and right ventricular wall motion index (2.2 +/- 0.4 to 1.5 +/- 0.5; p less than .001) in 18 patients who survived longer than 1 year. Fourteen of these patients underwent upright bicycle exercise while off beta-blocking drugs and peak radionuclide ejection fraction was acquired after anaerobic threshold was achieved. Right ventricular ejection fraction increased significantly from 41 +/- 10% to 47 +/- 12% (p less than .001), as did the left ventricular ejection fraction (55 +/- 15% to 60 +/- 12%; p less than .05). The direction and magnitude of change of the right ventricular ejection fraction correlated significantly with the left ventricular ejection fraction (r = .82, p less than .02). Deviations from this correlation occurred in patients who had a decreased forced expiratory volume in 1 sec and an abnormal ventilatory reserve during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rest and exercise ventricular function in adults with congenital ventricular septal defects

Rest and exercise right and left ventricular function were compared using equilibrium gated radionuclide angiography in 19 normal sedentary control subjects (mean age 28 years, range 22 to 34) and 34 patients with hemodynamically documented congenital ventricular septal defect (VSD) (mean age 27 years, range 20 to 40). The 34 patients with VSD were divided into 3 groups: those in Group 1 (17 patients) had pulmonary to systemic blood flow ratios of less than 2 to 1; those in Group 2 (12 patients) had prior surgical closure of VSD (mean interval from surgery 17 years, range 9 to 22), and those in Group 3 (5 patients) had Eisenmenger's complex. Gated radionuclide angiography was performed at rest and during each level of graded supine bicycle exercise to fatigue. Heart rate, blood pressure, maximal work load achieved, and right and left ventricular ejection fractions were assessed. The control subjects demonstrated an increase in both the left and right ventricular ejection fractions with exercise (0.70 +/- 0.07 to 0.79 +/- 0.05 and 0.46 +/- 0.06 to 0.57 +/- 0.04; p less than 0.001 for left and right ventricles, respectively). All study groups failed to demonstrate an increase in ejection fraction in either ventricle with exercise. Furthermore, resting left ventricular ejection fraction in Groups 2 and 3 was lower than that in the control subjects (0.59 +/- 0.09 and 0.54 +/- 0.06 versus 0.70 +/- 0.07; p less than 0.001) and resting right ventricular ejection fraction was lower in Group 3 versus control subjects (0.30 +/- 0.07 versus 0.46 +/- 0.06; p less than 0.001). Thus (1) left and right ventricular function on exercise were abnormal in patients with residual VSD as compared with control subjects; (2) rest and exercise left ventricular ejection fractions remained abnormal despite surgical closure of VSD in the remote past; (3) resting left and right ventricular function was abnormal in patients with Eisenmenger's complex; (4) lifelong volume overload may be detrimental to myocardial function.     

Beneficial effects of nitroglycerin on abnormal ventricular wall motion at rest and during exercise in patient with previous myocardial infarction.

The effects of sublingually administered nitroglycerin on segmental left ventricular wall motion determined by videotracking and radiographic left heart size were evaluated at rest and during submaximal hand grip exercise in 10 patients with previous transmural myocardial infarction. After nitroglycerin, diastolic left heart size decreased in the resting state from an average of 49.5 +/- 5.7 (standard deviation) to 47.9 +/- 5.6 mm/m2 body surface area (P less than 0.01) and during handgrip exercise from a mean of 50.7 +/- 590 to 49.1 +/- 4.7 mm/m2 (P less than 0.05). In the resting state, the average maximal velocity of shortening in segments with normal wall motion increased after nitroglycerin from 18.1 +/- 3.0 to 23.5 +/- 5.5 mm/sec (P less than 0.01), whereas during handgrip exercise alone, the velocity of shortening averaged 25.6 +/- 6.9 mm/sec and increased further after nitroglycerin to 30.1 +/- 10.6 mm/sec (P less than 0.05). The effects of nitroglycerin on the average extent of shortening in normal segments were similar. In all 10 patients, there was a decrease in the number of segments with abnormal wall motion. The number of sites with dyssynergy decreased after nitroglycerin from 24 to 15 in the resting state and from 40 to 22 when nitroglycerin was administered before handgrip exercise. Sublingually administered nitroglycerin appears to decrease left heart size, increase the velocity and extent of shortening in normal left ventricular segments and often reduce the extent of left ventricular wall motion abnormalities at rest and during isometric exercise in patients with previous transmural myocardial infarction.     

Effects of glucose-insulin-potassium infusion on the angina response during treadmill exercise.

The effects of glucose-insulin-potassium (GIK) and placebo normal saline (S) infusion on treadmill-walking time to angina, ST depression, heart rate (HR), systolic blood pressure (SBP), rate pressure product (RPP), blood glucose (G), lactate (L) and free fatty acids (FFA) were studied in 14 non diabetic patients with exertional angina. For the whole group, the post-GIK walking time to angina (393 +/- 33 sec, mean +/- SEM) was greater than the values during control GIK (319 +/- 20 sec, p less than 0.02) and post-S infusion (334 +/- sec, p less than 0.05), but circulatory and ST responses were similar in post-GIK and post-S studies. 7 of the 14 patients experienced significantly greater improvement in exercise tolerance following GIK (467 +/- 39 sec) in comparison to control GIK (313 +/- 29 sec, p less than 0.001) and post-S infusion (334 +/- 32 sec, p less than 0.005) and exercised to a higher HR, SBP and RPP after GIK than after S infusion. At the onset of angina these patients had similar ST-segment depression before and after GIK but when ST segments were assessed after GIK at the same exercise duration when angina had occurred during the control and post-S studies, there was significantly less ST depression (p less than 0.01). Of the remaining 7 patients exercise tolerance following GIK deteriorated in 3, remained unchanged in 2 and increased by 12 and 48 sec in 2 patients in comparison to post-S values. Comparison of post-GUK and post-S values for G, L and FFA for the whole group showed significantly lower resting values of FFA and post-exercise values of G following GIK infusion. The differences in clinical and circulatory responses between patients who improved and those who did not improve following GIK were not related to the angiographically determined severity of coronary artery disease or to GIK-induced metabolic changes. Results suggest that some patients with angina pectoris do benefit from GIK infusion but the response in a given patient to this therapeutic modality is unpredictable.     

Repeat balloon aortic valvuloplasty.

This paper attempts to determine limitations and indications of performing a second balloon aortic valvuloplasty procedure (BAV2) because of restenosis, which is the major limitation of this technique. From September 1985 to December 1989, 357 patients underwent a primary BAV (BAV1) and 67 patients had a BAV2. Forty-two patients (group A) had repeat catheterization because they were markedly symptomatic 11 +/- 7 months after BAV1. Twenty-five patients (group B) came from a group of 73 patients who had been systematically scheduled for repeat catheterization in order to evaluate the hemodynamic restenosis rate 8 +/- 3 months after BAV. At time of BAV2 most of the patients of group A were severely disabled. Comparison of pre-BAV2 gradient and aortic valve area with pre-BAV1 measurements showed in a slightly less severe degree of aortic stenosis in group A and in group B with any difference in cardiac index and ejection fraction. Immediately following BAV2, the gradient decreased from 72 +/- 22 to 33 +/- 15 mm Hg (P less than 0.001) and aortic valve area increased from 0.56 +/- 0.18 to 0.85 +/- 0.28 cm2 (p less than 0.001) in group A. In group B, gradient decreased from 68 +/- 15 to 33 +/- 15 mm Hg (p less than 0.001) and aortic valve area increased from 0.70 +/- 0.16 to 0.90 +/- 0.25 cm2 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Diastolic mechanisms for systolic dysfunction during exercise

Left ventricular ejection fraction is normal at rest but may respond abnormally to exercise in many patients with essential hypertension. To assess the determinants of the abnormal ejection fraction response to exercise, we performed radionuclide angiography at rest and during exercise in 41 hypertensive patients without coronary artery disease. In 22 patients (group 1), the ejection fraction increased more than 5% during exercise; in the other 19 patients (group 2), the ejection fraction either increased by less than 5% or decreased with exercise. Left ventricular diastolic filling was impaired at rest in patients in group 2 compared with group 1, with reduced peak filling rate (2.5 +/- 0.4 vs. 3.1 +/- 0.7 end-diastolic volume/sec; p less than 0.01) and prolonged time to peak filling rate (175 +/- 28 vs. 153 +/- 22 msec; p less than 0.01). Impaired diastolic filling in group 2 was associated with less augmentation in end-diastolic volume during exercise compared with group 1 (p less than 0.01). These observations were not dependent on the threshold value that was arbitrarily chosen to define an abnormal ejection fraction response, as there were significant correlations for the entire group between the magnitude of change in ejection fraction with exercise and both the resting peak filling rate (r = 0.46) and the change in end-diastolic volume with exercise (r = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)     

Daily variations of ECG and left ventricular parameters at exercise in patients with anginal attacks but normal coronary arteriograms

In 21 patients with typical exercise-induced anginal pain but normal coronary arteriograms (group N) and in 14 patients with angiographically proved coronary stenosis (group C), symptom-limited ergometer exercise ECG and radionuclide angiocardiography were performed twice on two different days. Exercise-induced ST changes showed larger variations between the two exercise tests in group N than in group C ([delta ST1-delta ST2]: 0.07 +/- 0.06 mV in group N, 0.03 +/- 0.03 mV in group C, p less than 0.05). Rate pressure product and left ventricular ejection fraction at exercise also showed larger variations between the two tests in group N than in group C (p less than 0.001, p less than 0.05, respectively). However, substantial overlaps existed in some cases in the two groups. In conclusion, some of the patients with exercise-induced anginal pain but normal coronary arteriograms may have a variable threshold of exertional chest pain probably caused by variation in coronary vascular tone, and the other patients may have a fixed threshold of chest pain caused by other mechanisms.     

The effects of aging after coronary arterial bypass grafting on the regulation of cardiac output during upright exercise

We examined the effects of age on cardiac performance and the mechanisms that regulate cardiac output during upright exercise in patients free of myocardial ischemia after coronary revascularization. There were 90 subjects, aged 36 to 75 years, of whom 27 were greater than or equal to 60 years. There were no age-related changes in resting heart rate, systolic blood pressure, left ventricular end-diastolic volume index, left ventricular end-systolic volume index, stroke volume index, cardiac index and left ventricular ejection fraction. There were, however, age-related changes in exercise capacity (y = 20 - 0.21x, r = -0.52, P less than 0.001); exercise heart rate (y = 185 - 1x, r = -0.42, P less than 0.001); exercise end-systolic volume index (y = 11 + 0.46x, r = 0.28, P less than 0.01) and exercise ejection fraction (y = 81 - 0.31x, r = -0.28, P less than 0.01). In a subgroup of 54 patients with comparable exercise workload (27 aged less than 60 and 27 greater than or equal to 60 years), the age-related differences in exercise end-systolic volume index, exercise ejection fraction and exercise cardiac index were not observed, but the exercise heart rate was still higher in the younger patients (y = 168 - 0.76x, r = -0.34, P less than 0.01). Thus, age modifies the compensatory mechanisms that regulate the cardiac output during exercise. Young and old patients alike show increases in end-diastolic volume and ejection fraction to maintain exercise cardiac output. The higher exercise heart rate in the younger subjects suggests a decrease in cardiac responsiveness to adrenergic stimulation associated with aging.     

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.     

Progressive improvement in pulmonary vascular resistance after percutaneous mitral valvuloplasty

Percutaneous mitral valvuloplasty has been proposed as a nonsurgical technique for treating high-risk patients with mitral stenosis who are deferred from mitral valve replacement. The effect of this technique on patients with pulmonary hypertension, however, has not been fully evaluated. Accordingly, serial assessment of pulmonary vascular resistance was made in 14 patients with critical mitral stenosis and pulmonary hypertension (pulmonary vascular resistance greater than 250 dynes.sec/cm5 or mean pulmonary artery pressure greater than 40 mm Hg or both) who underwent percutaneous balloon dilatation of the mitral valve. Balloon valvuloplasty was performed with either one (n = 10) or two (n = 4) balloons through the transseptal approach, and it resulted in significant improvement in mean mitral gradient (from 18 +/- 4 to 9 +/- 4 mm Hg, p less than 0.001), systemic blood flow (from 3.7 +/- 1.2 to 5.0 +/- 2.2 l/min, p less than 0.001), and calculated mitral valve area (from 0.7 +/- 0.2 to 1.6 +/- 0.7 cm2, p less than 0.001). Immediately after balloon mitral valvuloplasty, pulmonary vascular resistance fell from 630 +/- 570 to 447 +/- 324 dynes.sec/cm5. Repeat catheterization 7 +/- 4 months after valvuloplasty showed further improvement of pulmonary hypertension in 12 of the 14 patients, with a mean pulmonary vascular resistance for the group as a whole of 280 +/- 183 dynes.sec/cm5, p less than 0.005. In two patients, mitral valve restenosis to a mitral valve area less than 1.0 cm2 was associated with a return of pulmonary hypertension to predilatation values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical significance of perfusion defects by thallium-201 single photon emission tomography following oral dipyridamole early after coronary angioplasty

The clinical significance of myocardial perfusion defects present early after angiographically successful percutaneous transluminal coronary angioplasty was assessed in 53 patients using thallium-201 single photon emission computed tomography combined with pharmacologic vasodilation induced by a large dose (300 mg) of orally administered dipyridamole. Myocardial tomographic images were obtained at a mean of 20 +/- 6 h (SD) before and 2.9 +/- 2.7 days after angioplasty. Before angioplasty, 15 (28%) of the 53 patients developed angina after dipyridamole administration, in contrast to only 3 (7.5%) of 40 patients after angioplasty (p less than 0.001). The mean percent luminal area stenosis decreased from 93 +/- 6% before angioplasty to 34 +/- 17% after angioplasty (p less than 0.001). Myocardial perfusion defects, present in 49 (93%) of the 53 patients before angioplasty, were reversible in 44 patients (83%), all of whom underwent dilation of arteries supplying the ischemic areas. After angioplasty, 26 (65%) of 40 patients had no ischemic defects, whereas 14 (35%) of the patients still had an ischemic defect in the vascular territory of the dilated artery. After a mean follow-up period of 21.7 months, 13 (33%) of 39 patients developed restenosis, 10 of whom had an ischemic defect early after angioplasty. Restenosis developed in 10 (71%) of 14 patients with an ischemic defect after angioplasty, but in only 3 (11.5%) of the patients without an ischemic defect (p = 0.007). In conclusion, thallium-201 tomography after oral dipyridamole affords convenient assessment of the physiologic significance of coronary stenosis present before angioplasty and the residual stenosis after angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormal cardiac function in diabetic patients with autonomic neuropathy in the absence of ischemic heart disease

To determine if cardiac autonomic neuropathy (CAN) contributes to diabetic cardiomyopathy, left ventricular function was assessed by resting and exercise radionuclide ventriculography (RVG) in 30 patients with long-standing insulin-dependent diabetes mellitus who had no clinical, electrocardiographic, or tomographic thallium scan evidence of heart disease. In 11 of 30 patients (37%), RVG revealed abnormal left ventricular performance. CAN was found in 91% of these patients. RVG was abnormal in 59% of patients with CAN and in only 8% of patients without CAN (P less than 0.005). There were significant reductions in mean (+/- SE) ejection fractions (EF) in patients with CAN at rest (62.8 +/- 2.2% vs. 75.2 +/- 2.5%; P less than 0.001) and with maximal exercise (65.8 +/- 2.6% vs. 80.9 +/- 2.3%; P less than 0.001) compared to patients without CAN. There was an inverse correlation between the autonomic function score and both resting EF (r = -0.53; P less than 0.002) and exercise EF (r = -0.55; P less than 0.002). Systolic function did not correlate with age, sex, duration or control of diabetes, microvascular complications, or plasma norepinephrine levels. Thus, approximately one third of our study population had evidence for depressed left ventricular function in the absence of ischemic heart disease, and the cardiac dysfunction was related to the severity of CAN. CAN may be a contributor to cardiac dysfunction in diabetes mellitus.