Nitroglycerin and afterload: effects of aortic compliance and capacity of the Windkessel.
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Biomedical subjects
Publications and source records attributed to K L Neuhaus.
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Peak left ventricular ejection rate (dV/dtsyst) and peak left ventricular filling rate (dV/dtdiast) were determined from biplane cineangiographies in patients with normal left ventricular function (n = 8), pressure overload (n = 11), aortic regurgitation (n = 7), mitral regurgitation (n = 9), mitral stenosis (n = 6), hypertrophic obstructive cardiomyopathy (n = 10), congestive cardiomyopathy (n = 9) and coronary heart disease (n = 17). dV/dtsyst (normal 642 +/- 187 ml s-1) was reduced in mitral stenosis (447 +/- 77 ml s-1) and was increased significantly in aortic regurgitation (1085 +/- 162 ml s-1) and mitral regurgitation (744 +/- 232 ml s-1). dV/dtsyst/EDV was correlated linearly with ejection fraction and was reduced significantly in mitral stenosis, aortic and mitral regurgitation, congestive cardiomyopathy and coronary heart disease. Ventricles with pressure overload and coronary heart disease could be separated better from normal ventricles by dV/dstsyst/EDV than by ejection fraction. dV/dtdiast (normal 549 +/- 205 ml s-1) was decreased significantly in mitral stenosis and increased in aortic regurgitation (1141 +/- 557 ml s-1) and mitral regurgitation (946 +/- 349 ml s-1). Peak left ventricular filling rate and diastolic stiffness were correlated by a hyperbolic function. The results show that peak left ventricular ejection and filling rates allow a more detailed analysis of ventricular function than the usually applied parameters. Quantification of the factors which determine the rate of change of left ventricular volume was only partially possible.
The hemodynamic effects of the new vasodilator drug isobutyl methyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinecarboxylate (nisoldipine, Bay k 5552) were observed in 9 patients undergoing cardiac catheterization. The drug was administered i.v. in a dose of 1.5 microgram/kg body weight. Within 1 min after injection aortic pressure decreased by 11.5 +/- 6.4%, cardiac index increased by 23.1 +/- 13.5%, and heart rate accelerated by 18.3 +/- 10.1% of control value. Calculated total peripheral resistance was reduced by 28.2 +/- 10.1%. The whole low pressure system as well as the dp/dt max remained unaffected by the drug. The stroke volume index showed a slight and insignificant increase. Thus, Bay k 5552 represents a fast and power fully acting vasodilating substance with its actions being restricted mainly to the peripheral vasculature.
The effects of hypertrophy and dilatation on myocardial force and shortening were analysed using Wong's formula for equatorial midwall stress in a thick-walled ellipsoid of revolution. Wall thickness, chamber volume and ejection fraction were treated as independent variables. An isolated increase in wall thickness reduces wall stress and, to a lesser extent, myocardial fiber shortening, i.e. myocardial function is overestimated from ventricular pressures and ejection fraction. Ventricular dilatation without a proportional increase in myocardial mass leads to an increase of myocardial force and shortening, i.e. myocardial performance is underestimated from ventricular function. A decrease of ejection fraction increases total systolic myocardial force considerably, leading to a shift to the right on the inverse relation of force and shortening. Therefore the efficiency of myocardial contraction is reduced and myocardial performance is better than ventricular pump function would indicate.
Left ventricular and myocardial performance were analyzed in 9 patients with chronic volume overload by mitral regurgitation from biplane cineventriculograms, simultaneous pressure recordings and cardiac output (thermodilution method) determinations. In spite of a considerable regurgitant fraction (49 +/- 17% of total stroke volume) cardiac index on the average is normal (CI = 3.3 +/- 0.7 l . min-1). The main compensatory mechanism to maintain cardiac ouput in hypertorphy (WED = 1.1 +/- 0.2 cm; LVMI = 216 +/- 62 g . m-2; LVMI/EDVI = 1.3 +/- 0.3 g . ml-1) and dilatation (EDVI = 163 +/- 37 ml . m-2). An increase of preload is of minor importance (PLVED = 15 +/- 7 mmHg; sigma ED = (40 +/- 19) x 10(3) dyn . cm-2). Left ventricular enlargement and wall mass are related to the degree of clinical heart failure (NYHA). Enddiastolic volume on the average is more increased than total stroke volume (89 +/- 31 ml . m-2). Ejection fraction (EF = 54 +/- 7%) was depressed despite a normal afterload (sigma tej = (171 +/- 37 x 10(3) dyn. cm-2; sigma max = (247 +/- 48 x 10(3) dyn . cm-2). The reduced ejection fraction and diminished myocardial power are related to an impairment of myocardial function (VMW . sigma tej = (83 +/- 39) x 10(3) dyn . cm-2 . s-1; VMW . sigma tej/ln sigma ED = 7.9 +/- 3.6 x 10(3) dyn . cm-2 . s-1). In comparable degrees of heart failure myocardial function is more compromised in patients with mitral than with aortic regurgitation.
In a 60-year-old male patient thrombotic occlusion of a dominant right coronary artery was recanalized by means of a Sones-Catheter (8F) two hours after the clinical onset of myocardial infarction. Before recanalization the inferior wall of the left ventricle was akinetic. After recanalization this akinesia and the clinical symptoms of myocardial infarction was almost completely relieved. As evidenced by ECG and enzymes there was only a minor necrosis of the inferior wall. After one week ventricular function angiographically was completely normal. In the right coronary artery there was a 50 percent proximal stenosis, thrombi were completely abolished. Possible implications of this case are discussed.
The influence of chronic volume load on ventricular function and myocardial load and shortening was investigated in 10 patients with chronic aortic regurgitation by means of biplane ventriculography and simultaneous pressure measurements. The regurgitant fraction was 63 +/- 15 per cent. Enddiastolic volume (EDVI 227 +/- 37 ml/m2), systolic (161 +/- 18 mm Hg) and enddiastolic ventricular pressure (30 +/- 12 mm Hg) were elevated, ejection fraction was reduced (54 +/- 7 per cent). Myocardial mass related to EDV was normal (1.2 +/- 0.2 g/ml). Contractility as measured from dp/dt max (1736 +/- 492 mm Hg s-1) and dp/dtmax/PI (22.2 +/- 4.3 s-1) was slightly reduced. Mean velocity of equatorial midwall fiber shortening VMW 0.45 +/- 0.13 cir X s-1) was significantly diminished, equatorial midwall fiber stress during ejection (sigma tej 267 +/- 44.5 X 10(3) dyn X cm-2) was elevated. In spite of a very high enddiastolic stress (sigma ED 96 +/- 36 X 10(3) dyn X cm-2) mean systolic power (sigma tej X VMX 123 +/- 43.2 X 10(3) dyn X cm-2 X s-1) was normal. Compensation of chronic volume load in aortic regurgitation is not compensated by an increased contractility but by ventricular enlargement and a pronouned increase in preload. Myocardial load and shortening in chronic aortic regurgitation are altered in the same way (increased stress and reduced shortening) as in chronic pressure overload.
UNLABELLED: Left ventricular diastolic pressure-volume relations (PVR) were analysed from biplane ventriculograms and simultaneous pressure measurements in 33 patients at rest (R) and during ergometer exercise (E) (8 normals [N], 8 patients with coronary artery disease [CAD], 8 patients with congestive cardiomyopathy [COCM], 5 patients with aortic insufficiency [AI] and 5 patients with pressure overload (4 with aortic stenosis [A-St.] and 1 coarctation of the aorta). In N and AI diastolic PVR was essentially unchanged with E, the time constant of isovolumic relaxation (T) decreased significantly (N: delta T = -24.4 +/- 11.6%, p less than 0.001; AI: delta T = -27.3 +/- 6.8%, p less than 0.005). In CAD diastolic PVR was shifted upwards in all cases with angina pectoris during E (7/8), minimal rate of left ventricular pressure change (dp/dtmin) and T did not change significantly. In COCM diastolic PVR was shifted upwards in 4 cases, while dp/dtmin increased significantly (R = -1107 +/- 327, E = -1508 +/- 626 mm Hg-s-1, p less than 0.05), T on the average was unchanged (R = 53 +/- 10.5, E = 51 +/- 14.2 msec). In A-St. in 3 of 4 cases diastolic PVR was significantly shifted upwards with E, dp/dtmin increased (R = -1633 +/- 93, E = -2093 +/- 170 mm Hg-s-1, p less than 0.001), T in contrast to N and AI was prolonged (R = 33.8 +/- 4, E = 39.9 +/- 1.9 msec). CONCLUSION: In N and AI diastolic ventricular function is not altered with exercise. In COCM and especially in A-St., however, there are similar alterations like in CAD with angina pectoris. Changes in T indicate that shifts of the PVR with exercise in non-ischemic heart disease are related to a disturbed ventricular relaxation.
10 healthy men aged 18 to 32 years underwent M-mode-echocardiographic studies at rest, during exercise and recovery. Semisupine bicycle exercise was performed using work loads of 25, 50, 75, and 100 W with measurements taken every minute. With increasing exercise, heart rate rose significantly (p less than 0.01) from 68/min to a maximum of 132/min, blood pressure as obtained by sphygmomanometry rose from a mean of 83 torr to 102 torr. Left ventricular enddiastolic dimension (EDD) did not change significantly with exercise, left ventricular endsystolic dimension (ESD) decreased from a group mean of 34.8 mm to 30.5 mm. This paralleled an increase in stroke dimension from 18.3 to 22.6 mm and of fractional shortening (FS) from 0.34 to 0.43. Mean velocity of circumferential fiber shortening (MVCF) rose from 1.01 circ/s to 2.06 circ/s. During recovery, heart rate and blood pressure returned faster to resting levels than did ESD, FS, and MVCF. Again EDD did not change. These data indicate that heart rate contributes more to the increases in cardiac output observed with ergometric exercise than does stroke volume; with moderate exercise levels this increase in stroke volume is produced by diminishing endsystolic volume whilst enddiastolic volume remains unchanged.
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The influence of an instantaneous increase in afterload on the hemodynamics and regional myocardial function was studied in five anesthetized dogs before and after occlusion of the left anterior descending coronary artery. By inflation of an intaaortic balloon during single ejections, an instantaneous increase in afterload was obtained. From biplane cineventriculograms, the following parameters were calculated: left ventricular volumes (EDV, ESV), stroke volume (SV), ejection fraction (EF). Mean circumferential fiber shortening (V CF) was calculated in three ventricular diameters in the RAO projection. Simultaneously PLV, PLVED, PAo, and LV dp/dt were obtained. In the control ventriculograms, an increased afterload (delta PLV 16.4 +/- 8 mm Hg) caused only a minor decrease of SV (2.6 +/- 2.5 ml), EF (4.2 +/- 2.4%), and V CF (0.20 circ . s -1). After coronary occlusion (delta PLV 14.5 +/- 6.7 mm Hg),the reduction of SV (5.9 +/- 2.7 ml) and EF (8.2 +/- 2.6%) was more pronounced. This was caused mainly by a significant reduction of V CF in the center of ischemia (delta V CF -93%). For the evaluation of regional myocardial function by ventriculography, the marked influence of afterload in ischemic areas must be taken into consideration. This is of special interest in comparative ventriculograms, such as those before and after coronary bypass surgery.
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