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Biomedical subjects

O M Hess

Publications and source records attributed to O M Hess.

At least 163 records · Page 9Linked to original sources
PubMed1990

Dissecting aneurysm of the pulmonary artery with pulmonary hypertension.

Pulmonary artery dissection was observed in a 64-yr-old female patient with severe pulmonary hypertension, which was probably primary (pulmonary vascular resistance, 817 dyn.s.cm-5; normal range less than or equal to 200 dyn.s.cm-5). The patient was admitted to the hospital because of severe dyspnea on exertion. Echocardiography demonstrated a dissecting aneurysm of the pulmonary artery. Right heart catheterization revealed severe pulmonary hypertension (mean pulmonary artery pressure, 64 mm Hg; normal range, 10 to 22 mm Hg); dissection of the pulmonary artery was confirmed by pulmonary arteriography. One-year follow-up was uneventful. In the literature, 28 patients with dissecting aneurysm of the pulmonary artery are reviewed. The dissection has only been diagnosed in life in one patient (by echocardiography).

Aortic Dissection↗
PubMed1990

Effect of isradipine on left ventricular relaxation and diastolic filling.

The effect of two calcium antagonists on left ventricular (LV) relaxation and diastolic filling was evaluated in 16 randomized patients. Isradipine and nifedipine were administered intravenously in a maximum dose of 60 micrograms/min for isradipine and 63 micrograms/min for nifedipine. Heart rate was increased significantly (p less than 0.01) by both study agents. LV end-diastolic pressure remained unchanged whereas peak systolic pressure decreased significantly (p less than 0.01). The reduction in systolic pressure was significantly greater (p less than 0.05) after isradipine (delta P of 30 mm Hg) than after nifedipine (delta P of 13 mm Hg). The time constant decreased from 65 to 56 ms (p less than 0.05) after isradipine and from 62 to 59 ms (NS) after nifedipine. LV filling remained unchanged. It is concluded that both calcium antagonists are associated with a significant reduction in LV afterload accompanied by a reflex increase in heart rate. Isradipine is a more potent vasodilator than nifedipine at the same infusion rate. A beneficial effect on LV relaxation with isradipine, but not nifedipine, may be due to its less pronounced negative inotropic effect or its more potent afterload-reducing action.

Angiocardiography↗
PubMed1990

[Comparison of enalapril and captopril in the treatment of chronic heart failure].

The long-term effect of enalapril (group 1) and captopril (group 2) on clinical symptomatology and left ventricular function was evaluated in 29 patients with severe congestive heart failure (13 ischemic and 12 dilated cardiomyopathy, four valvular heart disease). During the 6-month observation period, five patients died (two on enalapril and three on captopril therapy = 6-month mortality rate 18%). Nine patients showed no beneficial effect of enalapril or captopril on clinical and hemodynamic findings (= nonresponders). The initial findings on these nine patients were, however, not significantly different from the clinical and hemodynamic findings on the patients who improved. Enalapril had to be discontinued in two patients because of side effects (progressive renal failure and gastrointestinal symptoms, respectively). A total of 22 patients completed the study, 11 treated with enalapril (mean dosage 25 +/- 10 mg/day) and 11 treated with captopril (mean dosage 77 +/- 26 mg/day). After 6 months there was a significant improvement according to the New York Heart Association (NYHA) classification, from 2.4 to 1.9 in group 1 (p less than 0.01) and from 2.7 to 1.9 in group 2 (p less than 0.001). The cardio-thoracic ratio (chest x-ray) decreased significantly from 0.59 to 0.56 (p less than 0.001) in group 1 and from 0.56 to 0.53 (p less than 0.001) in group 2. Physical working capacity (bicycle ergometry) showed a significant increase in both groups from 61% to 81% in group 1 (p less than 0.01) and from 66% to 83% in group 2 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1989

[Long-term course of hypertrophic cardiomyopathy: drug versus surgical therapy].

139 patients with hypertrophic cardiomyopathy (HCM) have been followed up for 1-28 years (mean 8.9 years). Group 1 consisted of 60 patients (mean age 38 years) without indication for septal myectomy (SM) (no pressure gradient at rest in 8, pressure gradient less than 50 mm Hg in 52 cases); group 2 consisted of 79 patients (mean age 36 years) who had SM (pressure gradient at rest 70 mm Hg). Management in group 1 was the following: (1a) propranolol (n = 20) (160 mg/d), (1b) verapamil (n = 18) (360 mg/d) and (1c) no therapy (n = 22). 19 patients died in group 1 (mortality 3.6% year); 17 died in group 2 (mortality 2.4%/year). 10 year survival in group 1b was 80% and in groups 1a und 1c 67% and 65% respectively. Patients of group 1b had a higher survival rate (p less than 0.05) than the other subgroups. Surgery patients treated with verapamil (120-360 mg/d) (n = 17) had a 10-year survival rate of 100% compared to 78% for surgery patients (n = 34) without such treatment (p less than 0.05). In summary, it can be said that the overall survival rate after SM is better than that with medical treatment. Under verapamil, however, survival is not different from that after surgery. The most favorable outcome was observed in surgery patients under long-term therapy with verapamil, probably due to the reduction of systolic pressure overload (SM) and improvement in diastolic function (verapamil).

Adult↗
PubMed1989

Effects of ischemia, bypass surgery and past infarction on myocardial contraction, relaxation and compliance during exercise.

Abnormalities of left ventricular function during ischemia have been described in animal models and in humans. Exercise, while a physiologic means of inducing ischemia, has a complex effect on left ventricular function by itself. In addition, patients with coronary artery disease have a diversity of chronic changes in myocardial structure and function. Therefore, with use of micromanometer left ventricular pressure measurements and ventricular volumes, calculated from biplane cineangiograms, left ventricular function at rest and during exercise was studied in 57 patients. Exercise-induced ischemia produced a decrease in ejection fraction, an increase in end-systolic volume, dramatic increases in diastolic pressures and an upward shift in the diastolic pressure-volume relation. Central to these changes was abnormal myocardial contraction and relaxation, with reduced regional shortening and impaired left ventricular pressure decay. However, nonischemic areas were capable of augmented shortening, and global pressure decay did accelerate slightly. These findings demonstrate that exercise-induced adjustments in contraction and relaxation are intertwined with ischemia-related abnormalities. Exercise studies in patients after bypass surgery and in patients with scars from distant myocardial infarction were useful in clarifying confounding factors. For example, asynchrony of contraction and relaxation, and chronic changes in passive chamber properties, also compromise systolic and diastolic function during exercise. In patients with coronary artery disease without ischemia during exercise, left ventricular end-diastolic pressure, but not early diastolic pressure, increased during exercise. The increase in pressure was appropriate for a slight increase in end-diastolic volume in a ventricle with a steep pressure-volume relation. Furthermore, end-systolic volume, while maintained during exercise, was not reduced, as occurs normally.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1989

On whether there is a true increase in myocardial stiffness during myocardial ischemia.

In the experimental animal, acute ischemia by interruption of coronary blood supply is accompanied by a steepening of the slope of the left ventricular pressure-volume and pressure-segment length relations. This increase in chamber stiffness is associated with an increase in myocardial stiffness assessed from the slope of the diastolic stress-strain relation. Supply-type ischemia in humans brought about by balloon inflation during coronary angioplasty leads to an upward shift of the pressure-length relation of the ischemic and the adjacent segment combined with a steepening of the slope. In demand ischemia produced by rapid pacing in patients with coronary artery disease, an increased radial stiffness modulus at any level of radial stress was present when compared with that during the resting state. These alterations of the stress-strain relation suggest that the physical properties of the myocardium change during both supply and demand ischemia. The increased diastolic myocardial stiffness appears to result, at least in part, from increased residual interaction between actin and myosin filaments.

Animals↗
PubMed1989

Functional and structural abnormalities in patients with dilated cardiomyopathy.

Passive diastolic properties of the left ventricle were determined in 10 control subjects and 12 patients with dilated cardiomyopathy. Simultaneous left ventricular angiography and high fidelity pressure measurements were performed in all patients. Left ventricular chamber stiffness was calculated from left ventricular pressure-volume and myocardial stiffness from left ventricular stress-strain relations with use of a viscoelastic model. Patients with dilated cardiomyopathy were classified into two groups according to the diastolic constant of myocardial stiffness (beta). Group 1 consisted of seven patients with a normal constant of myocardial stiffness less than or equal to 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a beta greater than 9.6. Structural abnormalities (percent interstitial fibrosis, fibrous content) in patients with dilated cardiomyopathy were assessed by morphometry from right ventricular endomyocardial biopsies. Heart rate was similar in the three groups. Left ventricular end-diastolic pressure was significantly greater in patients with cardiomyopathy (18 mm Hg in group 1 and 22 mm Hg in group 2) than in the control patients (10 mm Hg). Left ventricular ejection fraction was significantly lower in groups 1 (37%) and 2 (36%) than in the control patients (66%). Left ventricular muscle mass index was significantly increased in both groups with cardiomyopathy. The constant of chamber stiffness (beta*) was slightly although not significantly greater in groups 1 and 2 (0.58 and 0.58, respectively) than in the control group (0.35). The constant of myocardial stiffness beta was normal in group 1 (7.0; control group 6.9, p = NS) but was significantly increased in group 2 (23.5). Interstitial fibrosis was 19% in group 1 and 43% (p less than 0.001) in group 2 (normal less than or equal to 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (beta) and interstitial fibrosis (IF) (r = 0.95; p less than 0.001) and beta and fibrous content divided by end-diastolic volume index (r = 0.93; p less than 0.001). It is concluded that myocardial stiffness can be normal in patients with dilated cardiomyopathy despite severely depressed systolic function. Structural alterations of the myocardium with increased amounts of fibrous tissues are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. The constant of myocardial stiffness (beta) helps to identify patients with severe structural alterations (group 2), representing possibly a more advanced stage of the disease.

Adult↗
PubMed1989

Left ventricular pressure-length relation during exercise-induced ischemia.

The pressure-length relation in normal and ischemic segments was analyzed with use of left ventriculography and simultaneous micromanometry during supine exercise in 9 normal subjects and 12 patients with effort angina. Segmental analysis was done in the right anterior oblique projection using a long axis with three perpendicular, equidistant chords. The apical segment in the 12 patients with coronary artery disease represented the ischemic region. In 5 of the 12 patients with coronary artery disease, the basal segment that showed no exercise-induced deterioration in wall motion was used as an intrapatient control (nonischemic segment). In the 12 patients with coronary artery disease, left ventricular ejection fraction decreased (from 65% to 50%, p less than 0.001), end-diastolic pressure increased (from 24 to 40 mm Hg, p less than 0.001) and the lowest diastolic filling pressure increased (from 9 to 22 mm Hg, p less than 0.001) during exercise-induced ischemia. In normal subjects, ejection fraction increased (from 64% to 70%, p less than 0.01) with unchanged end-diastolic pressure, whereas the lowest diastolic filling pressure decreased during exercise (from 9 to 3 mm Hg, p less than 0.01). Global left ventricular diastolic pressure-volume curves showed an upward and rightward shift during exercise-induced ischemia. Regional pressure-length curves of both nonischemic (n = 5) and ischemic (n = 12) segments were shifted upward in early diastole, but moved to a higher portion of the rest pressure-length curve without an upward shift during mid- to end-diastole. In contrast, the apical segment in normal subjects showed a downward shift during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Bicycling↗
PubMed1989

[Normal values of left ventricular function. Biplanar angiocardiography with reference to sex-specific differences].

Normal values of left ventricular function have been determined in 24 patients by means of biplane angiocardiography. Global parameters were chamber volume, ejection fraction and muscle mass. Regional ventricular function was determined by means of an orthogonal and radial axial system. Radial axis shortening parameters showed smaller standard deviations and smaller coefficient of variations than orthogonal parameters. The smallest coefficient of variation elicited regional area reduction methods. Women showed significantly lower chamber volumes and muscle mass than men. There was no difference between the two sexes in the ejection fraction and wall thickness.

Adult↗
PubMed1989

Coronary vasomotor tone during static and dynamic exercise.

Coronary vasomotion is an important determinant of myocardial perfusion in patients with angina pectoris, and it influences not only normal but also stenotic coronary arteries. The ability of a stenotic coronary artery to change its size is dependent on the presence of a normal musculo-elastic wall segment within the stenosis (i.e., eccentric stenosis). Coronary vasoconstriction of normal and stenotic coronary arteries has been reported by Brown and coworkers (Circulation 1984; 70: 18-24) during isometric exercise. The effect of dynamic exercise on coronary vasomotion was evaluated in one group of 13 patients with ischaemia-like symptoms and normal coronary arteries (group 1) and in a second group of 12 patients with coronary artery disease with exercise-induced angina pectoris (group 2). Luminal area of a normal and a stenotic vessel segment was determined by biplane quantitative coronary arteriography at rest, during supine bicycle exercise and 5 min after administration of 1.6 mg sublingual nitroglycerin. Coronary sinus blood flow was measured in group 1 at rest and after 0.5 mg kg-1 intravenous dipyridamole using coronary sinus thermodilution. Coronary flow reserve was calculated from coronary sinus flow after dipyridamole divided by coronary sinus flow at rest. In group 1, coronary vasodilation of the large (i.e., proximal) and the small (i.e., distal) coronary arteries was observed during exercise in seven patients (subgroup A). However, in the remaining six patients (subgroup B) coronary vasoconstriction of the small arteries (-24%, P less than 0.001) was found during exercise, whereas the large vessels showed coronary vasodilation (+26%, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1989

Diltiazem alone and combined with nitroglycerin: effect on normal and diseased human coronary arteries.

The vasodilatory effect of diltiazem and nitroglycerin on the large epicardial coronary arteries was evaluated in 26 patients with coronary artery disease. The luminal area of a normal and a stenotic coronary artery was determined at rest, after intracoronary administration of diltiazem, during submaximal exercise as well as 5 min after 1.6 mg sublingual nitroglycerin using biplane quantitative coronary arteriography. Twelve patients with no pretreatment prior to the exercise test served as group 1 (controls) and 14 patients with intracoronary administration of 2 to 3 mg diltiazem prior to the exercise test as group 2. Normal vessel: In the control group luminal area increased significantly during exercise (+23%, P less than 0.01) and after sublingual administration of nitroglycerin (+40%, P less than 0.001). In group 2 luminal area increased after intracoronary administration of diltiazem (+19%, P less than 0.01), during bicycle exercise (+23%, P less than 0.001) and after sublingual administration of nitroglycerin (+39%, P less than 0.001). Stenotic vessel: In the control group luminal area decreased significantly (-29%, P less than 0.001) during bicycle exercise but increased after sublingual administration of nitroglycerin at the end of the exercise test (+12%, NS vs. rest). In group 2 intracoronary administration of diltiazem was associated with a mild increase in stenosis area (+11%, P less than 0.05). There was a further increase in stenosis area during bicycle exercise (+23%, P less than 0.001 vs. rest) and after sublingual nitroglycerin (+32%, P less than 0.001). Coronary vasodilation of the stenotic segment was, however, significantly more pronounced after sublingual nitroglycerin in group 2 than 1 (+32% versus 12%, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effect of intracoronary and intravenous propranolol on human coronary arteries.

The effect of intracoronary and intravenous propranolol on coronary vasomotion was evaluated in 28 patients with coronary artery disease. Luminal area of a normal and a stenotic coronary vessel segment was determined at rest, during submaximal bicycle exercise and 5 min after 1.6 mg sublingual nitroglycerin administered at the end of the exercise test involving biplane quantitative coronary arteriography. Patients were divided into three groups: group 1 (n = 12) served as the control group, group 2 consisted of 10 patients with intracoronary administration of 1 mg propranolol and group 3 of six patients with intravenous administration of 0.1 mg kg-1 propranolol prior to the exercise text. In the control group there was coronary vasodilation (+23%, P less than 0.01) of the normal and coronary vasoconstriction (-29%, P less than 0.001) of the stenotic vessel segment during bicycle exercise. After sublingual administration of 1.6 mg nitroglycerin there was vasodilation of normal (+40%, P less than 0.001 vs rest) and stenotic (+12%, NS vs rest) vessel segments. In group 2 intracoronary propranolol was not accompanied by a change in coronary vessel area but both normal (+13%, P less than 0.05) and stenotic (+22%, P less than 0.05) vessel segments showed coronary vasodilation during bicycle exercise. After sublingual nitroglycerin there was further vasodilation of both normal (+31%, P less than 0.001 vs rest) and stenotic (+45%, P less than 0.01 vs rest) arteries. In group 3 intravenous administration of propranolol was associated with a decrease in coronary luminal area of both normal (-24%, P less than 0.001) and stenotic (-31%, P less than 0.001) vessel segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Coronary stenosis vasomotion during dynamic exercise before and after PTCA.

Coronary vasomotion was evaluated in eight patients (age 50 +/- 8 years) with coronary disease before and 3.3 +/- 1.9 months after successful percutaneous transluminal coronary angioplasty (PTCA). Luminal area of a normal and a stenotic coronary artery was determined before and after PTCA using biplane quantitative coronary arteriography. Patients were studied at rest, during supine bicycle exercise and 5 min after 1.6 mg sublingual nitroglycerin. Workloads before and after PTCA were identical. Percentage diameter stenosis decreased from 78% to 24% (P less than 0.001) after PTCA. Mean pulmonary artery pressure increased during exercise from 21 to 40 mmHg (P less than 0.001) before and from 19 to 34 mmHg (P less than 0.001) after PTCA. Peak exercise pulmonary artery mean pressure was significantly (P less than 0.05) lower after PTCA. Normal coronary arteries showed a minimal increase in mean luminal area before (+2%; NS) as well as after (+6%; NS) PTCA. Nitroglycerin produced dilation of the normal vessel segment to a similar extent pre- (+27%; P less than 0.001) and post- (+31%; P less than 0.001) PTCA. In contrast, stenotic vessel segments showed coronary vasoconstriction during exercise before PTCA (-28%; P less than 0.01); after PTCA, exercise-induced vasoconstriction of the diseased segment was minimal (-4%; NS). Nitroglycerin was associated with vasodilation of the stenotic vessel segment before (+17%; NS) as well as after (+26%; P less than 0.005) PTCA. Thus, exercise-induced coronary vasoconstriction of stenotic coronary arteries is observed before as well as after PTCA, but vasoconstriction after PTCA is significantly less than before PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Abnormal coronary vasomotion during exercise in patients with normal coronary arteries and reduced coronary flow reserve.

A reduced coronary flow reserve has been reported in patients with ischemialike symptoms and normal coronary arteries. In 13 such patients, both coronary vasomotion and flow reserve were studied. The luminal area of the proximal and distal third of the left anterior descending and left circumflex artery were determined by biplane quantitative coronary arteriography using a computer-assisted system. Patients were studied at rest, during submaximal supine bicycle exercise (4.0 minutes, 116 W), and 5 minutes after sublingual administration of 1.6 mg nitroglycerin. Heart rate, mean pulmonary pressure, and mean aortic pressure as well as the percent change of both proximal and distal luminal area were determined. In 10 of the 13 patients, coronary sinus blood flow was measured by coronary sinus thermodilution technique at rest and after dipyridamole infusion (0.5 mg/kg in 15 minutes) 10 +/- 5 days after quantitative coronary arteriography. Coronary flow ratio (dipyridamole/rest) and coronary resistance ratio (rest/dipyridamole) were determined in these patients. Patients were divided into two groups according to the behavior of the coronary vessels during exercise (vasodilation, group 1; vasoconstriction, group 2). Coronary vasodilation of the proximal (luminal area +26%, p less than 0.001) and distal (+45%, p less than 0.001) artery was observed in seven patients (group 1) during exercise and after sublingual nitroglycerin (+46%, p less than 0.001; and +99%, p less than 0.001, respectively). In group 2 (n = 6), however, there was coronary vasoconstriction of the distal vessel segments (-24%, p less than 0.001) during exercise, whereas the proximal coronary artery showed vasodilation (+26%, p less than 0.001) during exercise. After sublingual nitroglycerin, both vessel segments elicited vasodilation (distal coronary, +44%, p less than 0.001; proximal coronary artery, +47%, p less than 0.001). Coronary flow ratio amounted to 2.5 in group 1 and 1.2 in group 2 (p less than 0.05) and coronary resistance ratio to 2.7 in group 1 and to 1.2 in group 2 (p less than 0.05), respectively. Thus, among patients with ischemialike symptoms and normal coronary arteries, there is a group of patients (group 2) with an abnormal dilator response of the distal coronary arteries to the physiologic dilator stimulus of exercise and a reduced dilator capacity of the resistance vessels after dipyridamole (abnormal coronary vasodilator syndrome). The nature of this exercise-induced distal coronary vasoconstriction is not clear but might be due to an abnormal neurohumoral tone that may cause or contribute to the blunted vascular response during exercise.

Angiography↗
PubMed1989

Left ventricular myocardial structure in aortic valve disease before, intermediate, and late after aortic valve replacement.

Left ventricular biplane cineangiography, micromanometry, and endomyocardial biopsies were performed in 27 patients with aortic stenosis (AS) and in 17 patients with aortic insufficiency (AI). Twenty-three patients with AS and 15 with AI were restudied at an intermediate time (18 months after successful valve replacement), and nine patients with AS and six with AI were restudied late (70 and 62 months after surgery). Biopsy samples were evaluated for muscle fiber diameter, percent interstitial fibrosis, and volume fraction of myofibrils. In control biopsy samples obtained from five donor hearts at transplantation, these morphometric variables averaged 21.2 microns, 7.0%, and 57.2%, respectively. After surgery, mass determined by cineangiography decreased from 186 to 115 and 94 g/m2 in patients with AS and from 201 to 131 and 93 g/m2 in patients with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and 28.7 microns in patients with AS and was 31.4, 27.6, and 26.4 microns in patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7% in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2 in patients with AS and from 42.1 to 28.9 and to 18.9 g/m2 in patients with AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the decrease of muscle mass determined by cineangiography at the intermediate time after valve replacement is mediated by regression of myocardial cellular hypertrophy in patients with AS and AI and in addition by a decrease of fibrous content in patients with AI. Late after surgery, left ventricular fibrous content also decreases in patients with AS. This late decrease associated with minor changes of end-diastolic volume may be important for improvement of increased diastolic myocardial stiffness. Even 6-7 years after valve replacement, incomplete regression of structural abnormalities of left ventricular hypertrophy still exists compared with the normal myocardium. The residually increased relative interstitial fibrosis and the small late postoperative decrease of volume fraction of myofibrils, associated with a prosthesis-related slight left ventricular pressure increase, are at the origin of a persistent systolic overload at the myofibrillar level.

Adult↗
PubMed1989

[Effect of intracoronary and intravenous administration of propranolol on coronary vasomotility at rest and during exercise].

The effect of intracoronary and intravenous propranolol on coronary vasomotion was evaluated in 30 patients with coronary artery disease. Luminal area of a normal and a stenotic coronary segment was determined at rest, during supine bicycle exercise and 5 min after 1.6 mg sublingual nitroglycerin administered at the end of the exercise test using biplane quantitative coronary arteriography. Patients were divided into 3 groups: Group I (n = 12) served as control Group II consisted of 10 patients with intracoronary administration of 1 mg propranolol and Group III of 8 patients with intravenous administration of 0.1 mg/kg propranolol prior to the exercise test. In the control Group there was coronary vasodilation (+23%, p less than 0.01) of the normal and coronary vasoconstriction (-29%, p less than 0.001) of the stenotic vessel segment during bicycle exercise. After sublingual administration of 1.6 mg nitroglycerin there was vasodilation of both normal (+40%, p less than 0.001 vs rest) and stenotic (+12%, NS vs rest) segments. In Group II intracoronary propranolol was not accompanied by a change in coronary area but both normal (+13%, p less than 0.05) and stenotic (+22%, p less than 0.05) segments showed coronary vasodilation during bicycle exercise. After sublingual nitroglycerin there was further vasodilation of both normal (+31%, p less than 0.001 vs rest) and stenotic (+45%, p less than 0.01 vs rest) arteries. In Group III intravenous administration of propranolol was associated with a decrease in coronary luminal area of both normal (-24%, p less than 0.001) and stenotic (-41%, p less than 0.001) segments. During dynamic exercise there was coronary vasodilation of both segments when compared to the data after intravenous injection of propranolol but there was no change in luminal area (normal vessel-2%, NS vs rest; stenotic vessel-3%, NS vs rest) when compared to the resting data. After sublingual administration of 1.6 mg nitroglycerin both normal (+21%, p less than 0.001) and stenotic (+46%, p less than 0.001) segments showed coronary vasodilation. It is concluded that supine bicycle exercise in patients with coronary artery disease is associated with vasodilation of the normal and vasoconstriction of the stenotic coronary arteries. Intravenous administration of propranolol is followed by coronary vasoconstriction of both normal and stenotic coronary arteries probably due to secondary mechanisms (reduction in heart rate and contractility) because it is not observed after intracoronary injection of propranolol and it is overridden by bicycle exercise and sublingual nitroglycerin.

Adult↗
PubMed1989

[Abnormal coronary vasomotility in subjects with normal coronary arteries and reduced reserve of coronary flow].

A reduced coronary flow reserve has been reported in patients with ischemia-like symptoms and normal coronary arteries. In 13 such subjects both coronary vasomotion and flow reserve were studied. The luminal area of the proximal and distal third of the left anterior descending and left circumflex artery were determined by biplane quantitative coronary arteriography using a computer-assisted system. Subjects were studied at rest, during submaximal supine bicycle exercise (4.0 min, 116 W) and 5 min after sublingual administration of 1.6 mg nitroglycerin. Heart rate, mean pulmonary and aortic pressure as well as the percent change of both proximal and distal luminal area were determined. In 10 of the 13 subjects, coronary sinus blood flow was measured by coronary sinus thermodilution technique at rest and after dipyridamole infusion (0.5 mg/Kg in 15 min) 10 +/- 5 days after quantitative coronary arteriography. Coronary flow ratio (dipyridamole/rest) and coronary resistance ratio (rest/dipyridamole) were determined in these subjects. Subjects were divided into 2 groups according to the behaviour of the coronary vessels during exercise (vasodilation = Group 1, vasoconstriction = Group 2). Coronary vasodilation of the proximal (luminal area + 26%; p less than 0.001) and distal (+ 45%; p less than 0.001) artery was observed in 7 subjects (Group 1) during exercise and after sublingual nitroglycerin (+46%; p less than 0.001 and +99%; p less than 0.001, respectively). In Group 2 (n = 6), however, there was coronary vasoconstriction of the distal vessel segments (-24%; p less than 0.001) during exercise, whereas the proximal coronary artery showed vasodilation (+ 26%; p less than 0.001) during exercise. Following sublingual nitroglycerin, both vessel segments elicited vasodilation (distal coronary + 44%; p less than 0.001, proximal coronary artery +47%; p less than 0.001). Coronary flow ratio amounted to 2.5 in Group 1 and to 1.2 in Group 2 (p less than 0.05) and coronary resistance ratio to 2.7 in Group 1 and to 1.2 in Group 2 (p less than 0.05), respectively. Thus, among subjects with ischemia-like symptoms and normal coronary arteries there is a subgroup of patients (Group 2) with an abnormal dilator response of the distal coronary arteries to the physiologic dilator stimulus of exercise and a reduced dilator capacity of the resistance vessels after dipyridamole (= abnormal coronary vasodilator syndrome). The nature of this exercise-induced distal coronary vasoconstriction is not clear but might be due to an abnormal neurohumoral tone which may cause or contribute to the blunted vascular response during exercise.

Adult↗