Biomedical subjects

H Nonogi

Publications and source records attributed to H Nonogi.

At least 127 records · Page 7Linked to original sources

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

Kinetic analyses of creatine kinase release patterns in patients with acute myocardial infarction undergoing emergency coronary arteriography.

To quantify the effects of early reperfusion on the size of infarcts, an enzyme indicator was developed: myocardial creatine kinase (CK) release rate (kr), based on a compartmental kinetics model. In 59 patients with acute myocardial infarction (MI) who received intracoronary thrombolysis therapy in the acute phase, the kr showed a good correlation with the flow condition of infarct-related coronary artery and the time required to reach peak enzyme activity. Apparent serum CK disappearance rate (kd') was estimated by using the method of Norris. The kd' was significantly underestimated in patients without reperfusion, suggesting the presence of prolonged enzyme release from the infarcted area. In 22 of 59 patients, who had a first acute anterior MI (left anterior descending arterial lesion), the correction of cumulative enzyme release by myocardial enzyme release (kr) resulted in a closer correlation with chronic phase left ventricular function. Thus, kinetic analyses of serum enzyme release provide a useful means to estimate the infarct size during intracoronary thrombolysis therapy.

Adult↗

PubMed1990

[Continuous monitoring of mixed venous oxygen saturation during exercise using fiberoptic pulmonary artery catheter].

We measured the mixed venous oxygen saturation (SvO2) continuously using a fiberoptic thermodilution pulmonary artery catheter to analyze the time course of SvO2 during exercise, and evaluated the relationship between SvO2 and exercise load, SvO2 and cardiac output. Five patients with old myocardial infarction and one healthy man underwent pulmonary arterial catheterization and then performed an incremental steady state exercise test using a supine cycle ergometer. There was a rapid fall in SvO2 43.4 +/- 10.6 seconds after the start of exercise and new steady state were achieved 92.6 +/- 22.5 seconds after changing the exercise load. The value of SvO2 at exercise load 60 watts were 44.7 +/- 9.8% and this value was under the level of lactic acid accumulation. SvO2 correlates well with cardiac output by the thermodilution method in individual patients. We conclude that a fiberoptic thermodilution pulmonary artery catheter was useful to evaluate the dynamic changes of SvO2 during exercise.

Adult↗

PubMed1989

Alterations in left ventricular relaxation, early diastolic filling and passive viscoelastic properties during postpacing ischemia.

Alterations in left ventricular relaxation, early diastolic filling, regional myocardial dynamics and passive viscoelastic properties during postpacing ischemia were studied in 9 patients with coronary artery disease. In all patients typical anginal pain developed during pacing tachycardia, and in the postpacing beat, left ventricular end-diastolic pressure increased from 14 +/- 4 to 26 +/- 5 mm Hg (mean +/- standard deviation, p less than 0.01), relaxation time constant increased from 44 +/- 9 to 59 +/- 7 ms (p less than 0.01) and ejection fraction diminished from 63.1 +/- 9.1 to 52.8 +/- 10.8% (p less than 0.01). However, peak rate of early left ventricular filling obtained from frame-by-frame analysis of left ventriculograms did not change significantly. The time difference from segmental peak lengthening to left ventricular peak filling increased significantly in the ischemic segment (32 +/- 30 vs 77 +/- 49 ms, p less than 0.05). Chamber stiffness constant of a viscoelastic model increased significantly from 0.0177 +/- 0.01 to 0.0354 +/- 0.015 (p less than 0.01) without change in chamber viscosity constant. In the ischemic segment, peak rate of lengthening decreased by 45% with ischemia, and peak rate of lengthening normalized for the end-diastolic segment length by 36%. However, peak rate of lengthening normalized for the extent of systolic shortening did not change. The control segment showed a tendency to increase in these 3 parameters, but the changes were not statistically significant. Thus, peak rate of segmental myocardial lengthening decreased with ischemia because of a decrease in segmental shortening.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

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

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

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↗

PubMed1988

[Coronary vasomotor activity; its significance for the therapy of angina pectoris].

Using quantitative biplane coronary arteriography, coronary vasomotion of normal and stenotic coronary artery segments was studied at rest and during supine bicycle exercise in 37 patients with coronary artery disease. Normal coronary arteries showed vasodilation during exercise, whereas stenotic arteries exhibited vasoconstriction. The occurrence of coronary stenosis narrowing during exercise can be explained either by a collapse of the free vessel wall due to an increase in coronary blood flow velocity (Venturi mechanism) or by insufficient production of the endothelium-derived vasorelaxing factor (endogenous nitrate). To explore further the nature of exercise-induced vasoconstriction of stenotic coronary arteries, intracoronary nitroglycerin, diltiazem or propranolol was given to a subgroup of patients prior to the exercise test. Administration of intracoronary nitroglycerin or diltiazem prevented exercise-induced vasoconstriction, probably due to the direct vasorelaxing effect of the drug on the smooth vasculature. Intracoronary administration of propranolol also prevented exercise-induced vasoconstriction, either due to a reduction in trans-stenotic pressure gradient (local beta blockade with a decrease in local coronary blood flow or an increase in distal arteriolar tone due to unopposed alpha-constrictor tone) or because of a local anesthetic effect of propranolol with a decrease in calcium influx into the smooth vasculature.

Angina Pectoris↗

PubMed1988

Prevention of coronary vasoconstriction by diltiazem during dynamic exercise in patients with coronary artery disease.

Whether exercise-induced vasoconstriction of coronary artery stenoses is modified by the administration of calcium antagonists was examined in 14 patients with classic angina pectoris. In this group the effect of intracoronary diltiazem (2 to 3 mg) on luminal area was evaluated in normal and stenotic segments of epicardial coronary arteries during symptom-limited supine exercise. The luminal area of a normal and a stenotic coronary artery segment was determined by quantitative coronary arteriography with a computer-assisted system. Patients were studied at rest, 6 min after 2 to 3 mg of intracoronary diltiazem, during supine bicycle exercise (96 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 normal and stenotic luminal area were determined. Intracoronary administration of diltiazem was associated with mild dilation of both normal (19%, p less than 0.01) and stenotic coronary luminal area (11%, p less than 0.05). During subsequent exercise, luminal area of the stenotic vessel segment increased by 23% (p less than 0.001) and that of the normal vessel segment by 24% (p less than 0.001), whereas in a previously reported control group, luminal area of the stenotic vessel segment decreased by 29% during exercise. After sublingual administration of nitroglycerin, the luminal area of both the normal and the stenotic vessel segment increased further by 19% (p less than 0.01) and 22% (p less than 0.01), respectively, compared with the values after intracoronary administration of diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗

PubMed1988

Left ventricular systolic series elastic properties in aortic stenosis before and after valve replacement.

In seven patients with aortic valve disease the time course of an auxotonic beat was compared with that of an isovolumetric beat produced by aortic cross clamping during open heart surgery. The rate of systolic stress rise (dS/dt; g.cm-2) of the isovolumetric beat at peak meridional wall stress (Sp; g.cm-2) of the auxotonic beat was determined by tipmanometry and simultaneous sonomicrometry and was found to be 87% of maximum dS/dt. In the second part of the study the stiffness index (k) was calculated in patients undergoing cardiac catheterisation according to: k = 0.87.(max.dS/dt)/Sp.Vcf, where Vcf = normalised midwall circumferential fibre shortening velocity (circ.s-1). In 22 patients, 10 controls and 12 patients with aortic stenosis before (pre) and after (post) valve replacement the systolic stiffness index k (circ-1) was determined using tipmanometry and frame by frame angiocardiography. Muscle fibre diameter and interstitial fibrosis were assessed from left ventricular endomyocardial biopsies. The systolic stiffness index k was 15 circ-1 in controls, 14 in preoperative patients with aortic stenosis and 12 (p less than 0.01 v controls) in postoperative patients. There was a significant correlation between k and muscle fibre diameter (r = 0.55; p less than 0.01) but not between k and interstitial fibrosis or ejection fraction. We conclude that systolic stiffness index k is normal despite marked left ventricular hypertrophy in preoperative patients with aortic stenosis. Following successful valve replacement systolic stiffness index decreased and was significantly lower than in controls. Series elasticity appears to be determined by structures related to the muscle cell rather than to interstitial fibrosis.

Aortic Valve Stenosis↗

PubMed1988

Left ventricular volume determination in dogs: a comparison between conductance technique and angiocardiography.

Left ventricular (LV) volume was determined simultaneously by monoplane cineangiocardiography and conductivity using a multielectrode conductance catheter at rest and during pressure loading in seven mongrel dogs (mean body weight 22 kg). LV volumes were calculated frame-by-frame (75 frames s-1) by angiocardiography and matched with instantaneous volumes obtained by conductivity. There was an excellent correlation between the two techniques at rest (correlation coefficient, r = 0.96) and during pressure loading (r = 0.92) when the data of each dog were pooled. The standard error of estimate of the mean angiographic volume was 4%. The slope of the regression analysis showed a small but significant (P less than 0.01) decrease from 0.365 at rest to 0.289 during pressure loading, whereas the intercept remained unchanged (24 versus 26 ml). Since no calibration for parallel conductivity of the surrounding tissue was performed, LV end-systolic volume was significantly over- and LV ejection fraction significantly underestimated whereas LV end-diastolic volume was estimated correctly by the conductance technique. It is concluded that LV end-diastolic volume can be determined accurately by the conductance technique in dogs. However, LV end-systolic volume is significantly over- and ejection fraction significantly underestimated. Since there is a good correlation between angiocardiography and conductivity, exact determination of LV volumes and ejection fraction is feasible using a correction factor. The change in slope of the regression equation between angiocardiography and conductivity suggests a change in conductivity of the surrounding tissue during pressure loading which limits the application of the conductance catheter to stable haemodynamic situations or calls for repeated calibrations by an independent technique during acute interventions.

Angiocardiography↗

PubMed1988

Diastolic properties of the normal left ventricle during supine exercise.

Diastolic function in response to dynamic exercise was studied by biplane left ventriculography and by measuring left ventricular pressure with a high fidelity micromanometer tipped catheter at rest and during supine bicycle exercise in nine normal subjects. During exercise there was a fall in end systolic volume, in the time constant of left ventricular isovolumic pressure decay, and in the lowest diastolic pressure. Stroke volume, peak filling rate, mean passive filling rate, and the volume at the lowest diastolic pressure increased. There was an increase in the number of time constants that had elapsed before the lowest diastolic pressure was reached and the slope of the pressure-volume curves during passive filling (delta P/delta V) increased without changes in end diastolic pressure and volume. These results show that during exercise elastic recoil is enhanced and left ventricular relaxation is faster and more complete. Both phenomena reduce the lowest diastolic filling pressure. The observed increase in chamber stiffness from rest to exercise is probably related to increased resistance of the left ventricular wall caused by higher passive filling rates. The enhanced early diastolic pressure decay during exercise allows stroke volume to increase despite an increase in diastolic viscoelastic resistance and chamber stiffness.

Adult↗

PubMed1988

Abnormal exercise hemodynamics in patients with normal systolic function late after aortic valve replacement.

We studied the hemodynamic response to supine bicycle exercise in 20 patients late (10 +/- 2 years) after aortic valve replacement (for aortic stenosis in 12 patients, aortic insufficiency in six patients, and for combined stenosis and insufficiency in two patients). The pulmonary artery wedge pressure was obtained with a pulmonary artery balloon catheter, and left ventriculography was performed by digital-subtraction angiography after injection of radiographic contrast into the pulmonary artery. These patients were compared with 11 control subjects with no or minimal cardiac disease studied routinely for evaluation of chest pain in whom left ventricular end-diastolic pressure and a direct contrast ventriculogram were obtained. Compared with the control population, the study population had similar left heart filling pressures (7 +/- 3 vs 9 +/- 3 mm Hg, NS), but higher left ventricular ejection fractions (75 +/- 7% vs 67 +/- 7%, p less than .02) and higher left ventricular muscle mass indexes (106 +/- 28 vs 85 +/- 9 g/m2, p less than .01). Elevated myocardial muscle mass led to lower systolic wall stress in the study population than in the control subjects (254 +/- 65 vs 320 +/- 49 10(3).dynes/cm2, p less than .01) and might explain the higher ejection fraction observed. Fourteen patients had a normal response to exercise (with left heart filling pressures of 16 +/- 4 vs 18 +/- 2 mm Hg for control subjects, NS; and left ventricular ejection fraction of 77 +/- 8% vs 73 +/- 5% for control subjects, NS). However, while the remaining six patients had a normal exercise left ventricular ejection fraction (72 +/- 9%, NS), they had an abnormal rise in left heart filling pressure (33 +/- 8 mm Hg, p less than .01). Preoperatively these patients also had higher left ventricular mid- and end-diastolic pressures at similar diastolic volumes, suggesting a decrease in chamber compliance. Thus, late after aortic valve replacement there is a subgroup of patients who, despite normal hemodynamics and normal left ventricular systolic function as assessed by the left ventricular ejection fraction at rest, have an abnormal response to exercise characterized primarily by a substantial rise in left heart filling pressures. Preoperatively this group also has a decrease in diastolic chamber compliance despite nearly normal left ventricular ejection fractions. This abnormality appears to result from a primary derangement of diastolic function that is not evident at rest.

Aortic Valve↗

PubMed1988

Myocardial structure in patients with exercise-induced ischemia.

Myocardial structure of left ventricular segments with recurrent myocardial ischemia was evaluated by morphometry and compared with that of segments with normal blood supply in 15 patients with exercise-induced myocardial ischemia. Left ventricular high-fidelity pressure measurements and simultaneous biplane angiocardiography were performed in patients at rest and during supine bicycle exercise. Left ventricular transmural biopsy samples were obtained during open heart surgery in a normally contracting region and in a region with exercise-induced de novo wall motion abnormalities. Transmural and endocardial and epicardial left ventricular muscle fiber diameter and interstitial nonmuscular tissue were determined by morphometry. Eight patients were restudied 8 months after successful bypass grafting. Heart rate and left ventricular end-diastolic pressure increased significantly preoperatively and postoperatively during exercise. However, left ventricular end-diastolic pressure was significantly higher preoperatively (33 mm Hg) during exercise than postoperatively (19 mm Hg; p less than .01). Left ventricular ejection fraction dropped significantly during exercise (63% vs 54%; p less than .001) before surgery but remained unchanged (64% vs 66%; NS) after revascularization. Regional axis shortening of the normokinetic region increased slightly during exercise pre- and postoperatively, but decreased in the hypokinetic region from 42% at rest to 25% during exercise (p less than .001) before surgery and from 47% at rest to 41% during exercise (p less than .05) after revascularization. Transmural muscle fiber diameter (normal less than or equal to 23 microns) was significantly larger in regions with exercise-induced ischemia (29.3 microns, p less than .025) than in normally contracting regions (27.3 microns). Interstitial nonmuscular tissue (normal less than or equal to 10%) was significantly increased in regions with exercise-induced wall motion abnormalities (19.8%) compared with normally contracting regions (15.5%; p less than .05). In the endocardial half of left ventricular segments with recurrent myocardial ischemia interstitial tissue was significantly increased (23.7%; p less than .01) compared with that in the epicardial half of the same segment (17.5%). It is concluded that structural alterations of the myocardium (muscle fiber hypertrophy and increased interstitial nonmuscular tissue) develop especially in the endocardial layers of the transiently ischemic myocardium with normal function at rest.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiocardiography↗