Biomedical subjects

O M Hess

Publications and source records attributed to O M Hess.

At least 145 records · Page 8Linked to original sources

PubMed1991

Long-term follow-up of medical versus surgical therapy for hypertrophic cardiomyopathy: a retrospective study.

In a retrospective analysis 139 patients with hypertrophic cardiomyopathy were followed up for 8.9 years (range 1 to 28 years). Patients were divided into two groups: Group 1 consisted of 60 patients with medical therapy and Group 2 of 79 patients with surgical therapy (septal myectomy). Groups 1 and 2 were subdivided according to the medical treatment. Group 1a received propranolol, 160 mg/day (n = 20); Group 1b verapamil, 360 mg/day (n = 18); and Group 1c, no therapy (n = 22). Group 2a received verapamil, 120 to 360 mg/day, after septal myectomy (n = 17) and Group 2b had no medical therapy after surgery (n = 62). In Group 1, 19 patients died (annual mortality rate 3.6%) and in Group 2, 17 patients died (mortality rate 2.4%, p = NS). Of the patients who died, approximately one half to two thirds in both Groups 1 and 2 died suddenly and the other one half to one third died because of congestive heart failure. The 10 year cumulative survival rate was 67% in Group 1, significantly smaller than that in Group 2 (84%, p less than 0.05). In the subgroups, the 10 year survival rate was 67% in Group 1a, 80% in 1b (p less than 0.05 versus 1a) and 65% in 1c (p less than 0.05 versus 1b). The 10 year survival rate was 100% in Group 2a (p less than 0.05 versus 1a, 1b, 1c) and 78% in Group 2b (p less than 0.05 versus 2a). It is concluded that cumulative survival rate is significantly better in surgically than in medically treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Bronchial neuroendocrine (carcinoid) tumor causing unilateral left-sided carcinoid heart disease.

A female patient suffering from a bronchial neuroendocrine tumor with unilateral left-sided carcinoid heart disease is reported. Repeated x-ray films of the chest showed a slowly growing lung tumor in the left lower lobe. The patient refused any diagnostic or therapeutic procedure to define the type of the tumor. During the follow-up of 24 years she developed severe mitral and moderate to severe aortic insufficiency, both invasively quantified by thermodilution techniques. During surgery for double valve replacement the patient died from left ventricular heart failure. Necropsy revealed the typical pattern of a bronchial neuroendocrine tumor without metastases. Examination of the heart disclosed the characteristic deposits of fibrous tissue on the cusps of both the mitral and the aortic valves whereas the right heart showed no abnormalities. Review of the literature suggests the unilateral left-sided carcinoid heart disease to be a very rare finding, its pathogenesis remains to be elucidated.

Aged↗

PubMed1991

Coronary vasomotion and coronary flow reserve during exercise.

Coronary vasomotion and coronary blood flow are important determinants of myocardial perfusion in patients with coronary artery disease. New digital angiographic techniques allow to study, not only the dimensions of a stenotic lesion (quantitative coronary arteriography), but also coronary flow reserve (parametric imaging). In a preliminary study both techniques were combined and coronary dimensions, as well as coronary flow reserve were determined in 15 patients (seven normals and eight patients with coronary artery disease) at rest, 45 s after 10 mg i.c. papaverine, during two levels of supine bicycle exercise, as well as 5 min after 1.6 mg sublingual nitroglycerin. Our results show that with modern digital subtraction techniques, not only stenosis geometry, but also coronary flow reserve can be determined at rest and during exercise conditions.

Adult↗

PubMed1991

Function and structure of the failing left ventricular myocardium in aortic valve disease before and after valve replacement.

Left ventricular (LV) cineangiography and endomyocardial biopsies were performed preoperatively in 49 patients (pts) with aortic stenosis (AS) and 35 pts with aortic insufficiency (AI). LV failure (group 1) was present in 15 pts with AS and 17 pts with AI. In these pts ejection fraction (EF) was less than 57% and either cardiac index was less than 2.5 L/min/m2 and/or LV end-diastolic pressure was greater than 20 mm Hg. Macroscopic LV hypertrophy was assessed by angiographic muscle mass (LMMI, g/m2). Morphometric evaluation of LV biopsies included the determination of muscle fiber diameter (MFD, mu), percent interstitial fibrosis (IF, %), volume fraction of myofibrils (VFM, %) and the calculation of LV fibrous content (FC, g/m2). Pts of group 1 and 2 were restudied 22.5 and 24.0 months, respectively, after successful aortic valve replacement. Preoperatively, group 1 pts had a significantly higher LMMI, MFD, and FC than did the patients in group 2 (non-failing group consisting of 34 pts with AS and 18 with AI). IF and VFM did not differ. After surgery EF increased significantly from 44% to 59% in group 1, whereas it remained unchanged in group 2 (66%). Although in both groups LMMI and MFD decreased significantly these quantities were increased after surgery in group 1 as compared to group 2. IF, VFM, and FC did not change significantly in group 1 after valve replacement. There was no difference in these latter three quantities between groups 1 and 2 after surgery. It is concluded that 1) macroscopic and microscopic hypertrophy is more marked in the failing than in the non-failing left ventricle, 2) left ventricular pump function is not related to percent interstitial fibrosis, and 3) at an intermediate time after aortic valve replacement pts with previously failing left ventricle show considerable improvement of ejection performance, but residual hypertrophy persists.

Angiography↗

PubMed1991

Left ventricular wall thickness measurements by magnetic resonance: a validation study.

Left ventricular (LV) wall thickness was determined by magnetic resonance (MR) in 15 patients (7 controls and 8 patients with coronary artery disease). End-diastolic (ed) and end-systolic (es) wall thickness were measured in a short axis view perpendicular to the LV long axis. Wall thickness measurements were compared to data obtained by digital subtraction angiography (DSA) and M-mode echocardiography (Echo). End-diastolic and end-systolic wall thickness were significantly overestimated by MR (34% and 37%, respectively) when compared to DSA. In contrast, LV end-diastolic and end-systolic chamber diameter were significantly underestimated by MR (25% and 30%, respectively) when compared to DSA. However, fractioned shortening was similar (all NS) for MR (48 +/- 22%), DSA (54 +/- 15%) and Echo (44 +/- 10%), respectively. The mean difference (= accuracy) and the standard deviation of difference (= precision) for LV wall thickness was 0.4 +/- 0.2 cm between MR and DSA, 0.4 +/- 0.3 cm between MR and ECHO and 0.03 +/- 0.1 cm between DSA and ECHO. The correlation of wall thickness between MR and DSA (correlation coefficient r = 0.74, p less than 0.001) and between MR and Echo (r = 0.70, p less than 0.001) was good although the standard error of estimate (SEE) was 17% for MR vs. DSA and 21% for MR vs. Echo. The corresponding SEE for chamber diameter was 16% between MR and DSA and 19% between MR and Echo, respectively. Intraobserver variability for wall thickness determination by MR was excellent (correlation coefficient r = 0.99, p less than 0.001) SEE of 4%. Interobserver variability was also good (correlation coefficient r = 0.90, p less than 0.001) with a SEE of 12%. It is concluded that LV wall thickness and chamber diameter (short axis plane) can be determined by MR with good precision but only satisfactory accuracy. LV wall thickness is significantly overestimated probably due to signals from static blood which might be indistinguishable from the subendocardium.

Angiography, Digital Subtraction↗

PubMed1991

Coronary reserve in patients with aortic valve disease before and after successful aortic valve replacement.

In patients with aortic valve disease and normal coronary angiograms coronary reserve was determined by the coronary sinus thermodilution technique. Three groups of patients were studied: 37 preoperative patients; 18 different patients 12-52 months after aortic valve replacement and seven control subjects with no cardiac disease. Coronary flow ratio (dipyridamole/rest) was diminished in preoperative compared with postoperative patients (1.66 +/- 0.44 vs 2.22 +/- 0.85; P less than 0.05) as well as with controls (2.80 +/- 0.84; P less than 0.01), and corresponding coronary resistance ratio (dipyridamole/rest) was higher in preoperative patients than in both other groups (0.61 +/- 0.17 vs 0.48 +/- 0.14; P less than 0.05 vs 0.37 +/- 0.10; P less than 0.01). Differences in the flow ratio, but not in the resistance ratio, were significant (P less than 0.05) in patients after aortic valve replacement compared with controls. Total coronary sinus blood flow at rest was elevated in preoperative compared with both postoperative patients and controls (252 +/- 99 vs 169 +/- 63; P less than 0.01; vs 170 +/- 35 ml.min-1, P less than 0.05), whereas flows after maximal vasodilation did not differ among the three groups (416 +/- 184 vs 361 +/- 150 vs 488 +/- 235 ml.min-1). Postoperative patients showed a distinct, though not total regression of left ventricular angiographic muscle mass index and wall thickness. Nine of the 18 postoperative patients showed a normal coronary flow reserve and nine showed subnormal response. These two subgroups did not differ with respect to preoperative macroscopic and microscopic measures of hypertrophy. Thus in aortic valve disease, the reduced coronary vasodilator capacity is mainly due to an elevated coronary flow at rest, while the maximal coronary blood flow achieved is identical to that of postoperative patients and controls. With regression of left ventricular hypertrophy, flow at rest decreases and this leads to a distinct improvement of coronary flow reserve.

Aged↗

PubMed1991

Determination of left ventricular systolic wall thickness by digital subtraction angiography.

The accuracy of digital subtraction angiography (DSA) for determination of left ventricular (LV) systolic wall thickness and muscle mass was evaluated in 20 patients (mean age 50 +/- 11 years). Conventional LV angiograms were digitized and subtracted using a combined subtraction mode ('mask mode' and 'time interval difference' subtraction). Wall thickness and muscle mass were determined at end-diastole, after the first- and second-third of systole and at end-systole. M-mode echocardiography (Echo), which was obtained from beam selection of the two-dimensional echocardiogram and conventional angiography (LVA), served as reference techniques. Angiographic LV wall thickness and muscle mass were determined according to the technique of Rackley in both, right (RAO) and left (LAO) anterior oblique projections, whereas echocardiographic wall thickness was measured just below the mitral valve orthogonal to the posterior wall (= LAO equivalent). Percent wall thickening was calculated in all patients. LV end-diastolic wall thickness and muscle mass correlated well between DSA and LVA (LV end-diastolic wall thickness in LAO projection r = 0.72, biplane LV end-diastolic muscle mass r = 0.83), LV end-systolic wall thickness (1.44 vs 1.33 cm, P less than 0.05) and percent wall thickening (52 vs 42%, P less than 0.05) compared favourably between echocardiography and DSA but was significantly larger when echocardiographically measured than with DSA (LAO projection). DSA and echocardiography showed a good correlation in regard to LV end-diastolic and end-systolic wall thickness (correlation coefficient r = 0.89, standard error of estimate SEE = 0.15 cm or 13% of the mean value).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Left ventricular passive diastolic properties in chronic mitral regurgitation.

BACKGROUND: In chronic mitral regurgitation, the myocardium responds to the increased filling volume by geometric alteration and eccentric hypertrophy. This study was designed to evaluate the effects of a pure volume overload on left ventricular diastolic chamber and myocardial properties and to assess the relation of passive diastolic function to systolic ejection performance. METHODS AND RESULTS: By use of simultaneous cineangiography and left ventricular micromanometry, left ventricular passive diastolic stiffness was evaluated in nine normal controls (group 1), 14 patients with chronic mitral regurgitation and a normal ejection fraction (greater than or equal to 57%, group 2), and 13 patients with mitral regurgitation and a reduced ejection fraction (less than 57%, group 3). Passive diastolic function was evaluated by using a three-constant elastic model. Left ventricular chamber properties were represented by the relation of pressure to volume; myocardial properties were evaluated by relating myocardial midwall stress to midwall strain. The constant of left ventricular chamber stiffness was decreased in group 2 compared with controls (p less than 0.05) but it was normal in group 3. The constant of myocardial stiffness was increased in group 3 compared with groups 1 and 2 (p less than 0.01). Among patients with mitral regurgitation, there was a significant inverse relation between ejection fraction and the constant of myocardial stiffness (r = -0.83). CONCLUSIONS: The chronic adaptation to volume overload in chronic mitral regurgitation tends to decrease left ventricular chamber stiffness. Patients with mitral regurgitation and a depressed ejection fraction demonstrated diastolic myocardial dysfunction. Compromised diastolic function in patients with chronic mitral regurgitation and reduced systolic performance may contribute to the clinical manifestations of congestive heart failure.

Adaptation, Physiological↗

PubMed1991

Diastolic function in valvular heart disease.

Diastolic dysfunction in patients with valvular heart disease is characterized by an impaired isovolumic relaxation, a normal or even enhanced early diastolic filling rate and an increased myocardial stiffness. These abnormalities do not depend on coexisting systolic dysfunction but are often combined. Several mechanisms are responsible for the occurrence of diastolic dysfunction, such as increased wall stress, altered myocardial structure, subendocardial hypoperfusion and/or diastolic calcium overload. Postoperative regression of myocardial hypertrophy is beneficial in regard to wall stress, subendocardial hypoperfusion and calcium overload but diastolic dysfunction might become worse after valve replacement due to a relative increase in interstitial fibrosis consequent to the decrease in myocyte mass (= myocardial remodeling). Persisting diastolic dysfunction with a substantial rise in left ventricular filling pressure can be observed during dynamic exercise in postoperative patients with preoperative severe pressure overload hypertrophy. Thus, diastolic dysfunction can be present as a primary derangement of cardiac function and can be unmasked as an abnormal response of diastolic filling pressure during exercise.

Cardiomegaly↗

PubMed1990

[Pathophysiology of heart insufficiency].

Chronic heart failure is characterized by the inability of the heart to pump the blood at a rate commensurate with the requirements of the peripheral organs at rest and under exercise conditions. The most common cause of heart failure is coronary artery disease, followed by hypertensive, valvular and myocardial heart disease. Different forms of chronic heart failure have been described (acute and chronic heart failure, forward and backward failure, right and left heart failure, systolic pump and diastolic compliance failure, etc.). The compensatory mechanisms in heart failure are related to hemodynamic and structural as well as metabolic and neurohumoral changes. Prognosis of chronic heart failure is usually poor and the annual mortality rate ranges between 20 and 50% depending on the degree of functional impairment.

Arrhythmias, Cardiac↗

PubMed1990

[Angina pectoris--drug therapy and costs in a medical outpatient clinic in Switzerland].

Prescriptions and costs of pharmacotherapy for exertional angina pectoris were studied in males treated in 1975, 1980 or 1985 at the outpatient clinic of the university of Zürich. Monotherapy was increasingly replaced by two drug regimens (1975 43%, 1980 59%, 1985 35%) or by triple therapy (1975 2%, 1980 10%, 1985 28%) respectively. In 1985 beta-blocking agents and calcium antagonists were more frequently used instead of nitrates in monotherapy. In combined treatment modalities, nitrates associated with calcium antagonists or calcium antagonists combined with beta blockers were used increasingly in 1985. The most used substances in 1985 were isosorbide dinitrate, atenolol and nifedipine. In 1985 nonselective beta blockers (propranolol, pindolol) were administered almost exclusively. The number of tablets administered per day decreased slightly over the years, while the doses of most commonly prescribed drugs increased. The cost per patient doubled during the observation period. Pharmacotherapy of stable angina calculated on the basis of 1985 pharmacy prices rose from 577 SFr. in 1975 to 1180 SFr. in 1985.

Adrenergic beta-Antagonists↗

PubMed1990

The poststenotic vessel segment during dynamic exercise: effect of oral isosorbide-dinitrate.

Coronary vasomotion of normal, stenotic, and poststenotic vessel segments was studied in 18 patients with coronary artery disease at rest, during submaximal bicycle exercise, and 5 min after sublingual nitroglycerin or oral isosorbide-dinitrate (ISDN) spray. Patients were divided into two groups: group 1 consisted of 10 patients with no premedication prior to exercise, and group 2 consisted of 8 patients receiving 120 mg long-acting ISDN orally 1 h before the procedure. Quantitative coronary arteriography was carried out in biplane projection using a semi-automatic computer system. The normal vessel segment showed a trend toward a small increase in cross-sectional area during exercise in both groups (+3% in group 1 and +4% in group 2, both NS). After sublingual nitroglycerin following exercise, there was a significant increase in group 1 (+29%, p less than 0.001 vs rest) but not after ISDN spray in group 2 (+5%, NS vs rest). The stenotic vessel segment showed exercise-induced stenosis narrowing in group 1 (-31%, p less than 0.01 vs rest) which was prevented by oral ISDN (+6%, NS vs rest). After exercise, sublingual administration of nitroglycerin or ISDN spray was associated with no significant change in stenosis area in either group. The poststenotic vessel segment showed no significant vasomotion during exercise in both groups (area change +6% in group 1 and +7% in group 2), but poststenotic luminal area increased after sublingual nitroglycerin (group 1: +15%, p less than 0.01 vs rest) or ISDN spray (group 2: +15%, p less than 0.05 vs rest). The mean pulmonary artery pressure increased during exercise from 22 to 39 mmHg (p less than 0.001) in group 1 and from 14 to 27 mmHg (p less than 0.001) in group 2. At rest (p less than 0.001) and during exercise (p less than 0.01) mean pulmonary pressure was lower in group 2 than in group 1. Thus, it is concluded that coronary vasomotion of the poststenotic vessel segment is only minimal during exercise and is not affected by coronary vasomotion of the stenotic vessel segment. Pretreatment with oral ISDN did not influence coronary vasomotion of the poststenotic vessel segment, but prevented exercise-induced stenosis narrowing. In the untreated patients, vasoconstriction of the stenotic vessel segment is limited to the site of the stenosis, and it appears that there is no release of vasoactive substances with vasoconstrictive influences on the poststenotic segment.

Administration, Oral↗

PubMed1990

Validation of a new automatic system for biplane quantitative coronary arteriography.

In a collaboration between the University of Texas (software) and the University of Zürich (hardware) a compact, automatic system for biplane quantitative coronary arteriography was developed. The system is based on a 35 mm film projector, a slow-scan CCD-camera (image digitizing) and a computer workstation (Apollo DN 3000, image storage and processing). A new calibration procedure based on two fixed reference points in the center of the image intensifier was used (isocenter technique). Contour detection of coronary arteries was carried out in biplane projection using a geometric-densitometric edge-detection algorithm. The proximal and distal luminal areas, as well as the minimal luminal area of the stenotic vessel segment were determined. Accuracy and precision were determined from precision drilled holes in a plexiglas cube which were filled with 50%, 75% and 100% contrast medium. The diameter of the holes ranged from 0.5 to 5.0 mm. The mean difference and the standard deviation of the differences between the true and the measured diameters were 0.12 +/- 0.14 mm for plane A and 0.26 +/- 0.17 mm for plane B, respectively. After a second order correction the mean difference amounted to 0.02 +/- 0.09 mm for plane A and 0.02 +/- 0.12 mm for plane B, respectively. Intra- and interobserver variability were evaluated in 5 patients (age 60 +/- 10 years) with coronary artery disease using 16 normal and 5 stenotic vessel segments (cross-sectional area ranging from 0.8 to 8.7 mm2). Two independent observers analyzed the same vessel segment twice. Intraobserver variability expressed as the standard error of estimate in percent of the mean angiographic vessel area (SEE) amounted to 2.1% for observer 1 and 4.4% for observer 2, respectively. Interobserver variability expressed as SEE was 4.1% for measurement 1 and 3.6% for measurement 2, respectively.

Aged↗

PubMed1990

Estimation of left-ventricular systolic performance and its determinants in man from pressures and dimensions of one beat: effects of aortic valve stenosis and replacement.

Within a thick heart-chamber wall, there is a midwall element or layer whose displacements best express systolic performance. The volume enclosed by that midwall element (Vm) and the average stress in that element (sigma m) can be calculated accurately by simple formulae. From simultaneous left-side pressure tracings and contrast cine-ventriculograms, Vm and sigma m were calculated at 20-ms intervals for an entire cardiac cycle in five normal subjects and in eight patients before and one year after replacement of stenotic aortic valves. Prior to surgery, the overloaded left ventricles were not hypertrophied enough to restore normal mid- and end-ejection stresses. Four had subnormal cavity ejection fractions, but all had subnormal midwall ejection fractions. All had subnormal fractional midwall ejection rates and prolonged active intervals (from the beginning of activation to the end of deactivation). Judging from pre-ejection pressure-development rates, the pressure-developing ability was not consistently elevated by concentric hypertrophy, because the stress-developing ability (contractility) was usually subnormal. The ability to shorten in the absence of afterload appeared to be subnormal in about half of the cases. The subnormal midwall ejection fractions appeared to be due to various combinations of increased mid- and late-ejection stresses, reduced contractility, and reduced shortening ability. On average and in several cases, reduced shortening ability appeared to be the main cause of the reduced performance. The effect of the slowed fractional midwall ejection rate to reduce the midwall ejection fraction was partially compensated by a prolonged active interval, by prolonged ejection time relative to the active interval, and by a more sustained ejection rate. Valve replacement partially restored all values except contractility towards normal, but the restorations of wall/cavity ratio and active interval were slight.

Adult↗

PubMed1990

Right ventricular diastolic function during exercise: effect of ischemia.

The effects of exercise on right ventricular diastolic function were evaluated in 14 patients who underwent supine rest and exercise right ventricular angiography. On the basis of coronary anatomy and exercise left ventricular regional wall motion analysis, these patients were classified into two groups: Group 1 (n = 7) had no or only mild coronary artery disease and Group 2 (n = 7) had significant coronary disease and exercise-induced left ventricular wall motion abnormalities suggesting ischemia. Chamber stiffness at rest was higher in Group 2 (48 x 10(-3) ml-1/m2) than in Group 1 (18 x 10(-3) ml-1/m2, p = 0.006). During exercise, right ventricular filling rate in the second half of diastole was significantly lower in Group 2 (126 versus 276 ml/m2 per s, p less than 0.03). The time constant of right ventricular pressure decay decreased significantly in both groups with exercise; however, both groups displayed a parallel upward shift of the pressure-volume curve with exercise. Because ischemia could not be demonstrated in Group 1, it is an unlikely explanation for this shift. Septal shifting was not a significant factor with exercise. Because of an increase in left ventricular end-diastolic volume with exercise and a close correlation between right and left ventricular end-diastolic pressures (r = 0.96 for Group 1 and r = 0.76 for Group 2), pericardial constraint is the most likely cause for this upward shift of the pressure-volume curve. Therefore, an increase in right ventricular end-diastolic pressure may not be a reliable indicator of ischemia during exercise because this pressure is coupled to changes in left ventricular volume and pericardial constraint.

Angiocardiography↗

PubMed1990

Potential role of coronary vasoconstriction in ischaemic heart disease: effect of exercise.

Coronary vasomotion plays an important role in the regulation of coronary perfusion at rest and during exercise. Normal coronary arteries show coronary vasodilation of the proximal (+20%) and distal (+40%) vessel segments during supine bicycle exercise. However, patients with coronary artery disease show exercise-induced vasoconstriction of the stenotic vessel segments. The exact mechanism of exercise-induced stenosis narrowing is not clear but might be related to a passive collapse of the disease-free vessel wall (Venturi mechanism), elevated plasma levels of circulating catecholamines, an insufficient production of the endothelium-derived vasorelaxing factor or increased platelet aggregation due to turbulent blood flow with release of thromboxane A2 and serotonin. Various vasoactive drugs, such as nitroglycerin and calcium antagonists, prevent exercise-induced stenosis vasoconstriction. An additive effect on coronary vasodilation of the stenotic vessel segment was observed after combination of nitroglycerin with diltiazem. Thus, exercise-induced stenosis narrowing plays an important role in the pathophysiology of myocardial ischaemia during dynamic exercise. The antianginal effect of vasoactive substances can be explained--besides the effect on pre- and afterload--by a direct action on coronary stenosis vasomotion.

Angiography↗

PubMed1990

Effect of intravenous propranolol on coronary vasomotion at rest and during dynamic exercise in patients with coronary artery disease.

Coronary vasomotion was studied at rest and during bicycle exercise with biplane quantitative coronary arteriography in 28 patients with coronary artery disease. Patients were divided into two groups; the first 18 patients served as controls (group 1), and the next 10 patients were treated with propranolol 0.1 mg/kg, which was infused intravenously before exercise (group 2). Luminal area of a normal and a stenotic vessel segment was determined at rest, during supine bicycle exercise, and 5 minutes after sublingual administration of 1.6 mg nitroglycerin after exercise. In group 1, the normal vessel showed vasodilation (+16%, p less than 0.001) during exercise, whereas the stenotic vessel segment showed vasoconstriction (-31%, p less than 0.001). After sublingual administration of nitroglycerin, there was coronary vasodilation of both normal (+36%, p less than 0.001 vs. rest) and stenotic (+20%, p less than 0.001) vessel segments. Patients with angina pectoris during supine exercise (n = 10) had significantly (p less than 0.05) more vasoconstriction (-36%) than patients without angina (-23%). In group 2, intravenous administration of propranolol at rest was associated with a decrease in luminal area of both normal (-24%, p less than 0.001) and stenotic (-43%, p less than 0.001) vessel segments; however, during subsequent exercise, both normal (-2%, p = NS vs. rest) and stenotic (-3%, p = NS vs. rest) vessel segments dilated when compared with the measurements after propranolol. Administration of nitroglycerin further increased luminal area of both vessel segments (normal segment, +23%, p less than 0.001; stenotic segment, +46%, p less than 0.001 vs. rest). It is concluded that dynamic exercise in patients with coronary artery disease is associated with coronary vasodilation of the normal and vasoconstriction of the stenotic coronary arteries. Patients with exercise-induced angina had significantly more stenosis vasoconstriction than patients without angina although minimal luminal area at rest was similar. Intravenous administration of propranolol is accompanied by a significant decrease in coronary luminal area of both normal and stenotic vessel segments at rest, which is overridden by dynamic exercise and sublingual nitroglycerin. The reduction in myocardial oxygen consumption and the prevention of exercise-induced stenosis vasoconstriction might explain the beneficial effect of beta-blocker treatment in most patients with coronary artery disease.

Adult↗

PubMed1990

Determination of coronary flow reserve by parametric imaging.

Nine mongrel dogs were instrumented with electromagnetic flow probes (EMF) to measure coronary blood flow through the left anterior descending (LAD) and left circumflex (LCx) coronary arteries at rest and after maximal coronary vasodilation (1 mg/kg/min adenosine). Relative coronary blood flow was determined by parametric imaging in the left posterior oblique projection using digital subtraction angiography (DSA). Transmural myocardial perfusion of the LAD and LCx beds was determined with tracer-labeled microspheres. Coronary flow reserve (maximal coronary blood flow divided by resting blood flow) was calculated under control conditions and after constriction of the proximal LAD or LCx by a screw occluder. Heart rate decreased significantly from 140 beats/min at rest to 122 beats/min after adenosine (p less than 0.001) and from 134 (rest) to 120 beats/min (adenosine; p less than 0.05) after coronary constriction. Peak systolic pressure was kept constant with an aortic constrictor. Left ventricular end-diastolic pressure increased significantly from 18 mm Hg at rest to 23 mm Hg (p less than 0.05) after coronary constriction. At baseline, coronary flow reserve was 4.2 with DSA, 3.8 with EMF, and 3.7 with microspheres; after coronary constriction, it was 2.6 (DSA), 1.9 (EMF), and 1.5 (microspheres) (all p less than 0.001 versus baseline). Coronary blood flow showed a good correlation between EMF and microspheres (r = 0.87, p less than 0.001), with a standard error of estimate (SEE) of 0.78 ml/g/min. Coronary flow reserve also showed a good correlation between EMF and microspheres (r = 0.82, p less than 0.001), with an SEE of 0.93. There was a moderate correlation between EMF and DSA (r = 0.68, p less than 0.001), with an SEE of 1.35 (40% of mean coronary flow reserve). The correlation coefficient between microspheres and DSA was 0.54 (p less than 0.01), with an SEE of 1.46 (39% of mean coronary flow reserve). The mean difference (accuracy) and standard deviation of difference (precision) were 0.2 +/- 1.0 between EMF and microspheres, -0.1 +/- 1.4 between EMF and DSA, and -0.6 +/- 1.7 between microspheres and DSA. We conclude that determination of coronary flow reserve by parametric imaging is associated with large variations that are greater than variations also inherent in the two reference techniques. Parametric imaging allows relatively accurate assessment of coronary flow reserve (small mean difference), but precision is low (large standard deviation of mean differences).(ABSTRACT TRUNCATED AT 400 WORDS)

Angiography, Digital Subtraction↗