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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<0.05) as well as with controls (2.80±0.84; P<0.01), and corresponding coronary resistance ratio (dipyridamolej rest) was higher in preoperative patients than in both other groups (0.61±0.17 vs 0.48±0.14; P<0.05 vs 0.37±0.10; P<0.01). Differences in the flow ratio, but not in the resistance ratio, were significant (P<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<0.01; vs 170±35 ml.min−1, P<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

Left ventricular (LV) wall thickness and muscle mass are important measures of LV hypertrophy. In 24 patients LV end-diastolic wall thickness and muscle mass were determined (two observers) by digital subtraction angiocardiography (DSA) and conventional LV angiocardiography (LVA). Wall thickness was determined over the anterolateral wall of the left ventricle according to the technique of Rackley (method 1) or by planimetry (method 2). Seventeen patients were studied at rest and seven during dynamic exercise. Wall thickness correlated well between LVA and DSA; the best correlations were obtained by a combined subtraction mode using either method 1 or 2 (method 1, r≥0-80; method2, r≥0. 75). The standard error of estimate of the mean (SEE) was slightly lower for method 2 (≤ 10%) than for method 1 (≤ 13%). DSA significantly overestimated wall thickness by 5-7% with method 1 and underestimated by 12-14% with method 2. Muscle mass correlated well between LVA and DSA; the SEE was ≤ 15% for method 1 and≤ 12% for method 2. Overestimation of muscle mass by DSA was 7-11% with method 1 and underestimation was 13-15% with method 2.It is concluded that LV wall thickness can be determined accurately by DSA with an SEE ranging between 10 and 13%. Determination of LV muscle mass is slightly less accurate and the SEE is slightly larger ranging between 13 to 17%. With method 1, wall thickness and muscle mass were over estimated and with method 2 underestimated

Objective: The aim was to assess the effect of nisoldipine on left ventricular systolic and diastolic function during prolonged myocardial ischaemia. Methods: The left circumflex coronary artery was ligated for 2 h and reperfused for 4 h in 12 calves. The animals were randomised to a control group (n=6) or to treatment with 1.25 mg·h−1 intravenous nisoldipine (n=6) during 2 h of ischaemia. Circulatory support by a ventricular assist device was performed throughout the experiment except for the time of haemodynamic measurements. Regional wall thickening of a normal and an ischaemic left ventricular region was determined using pairs of ultrasonic crystals. Left ventricular pressure was measured by micromanometry. Left ventricular wall thickness and regional wall stiffness at a common preload of 10 mm Hg were calculated using an elastic model with shifting asymptote. Results: Ten animals survived after 6 h. No difference was observed in systolic function between controls and nisoldipine treated animals. Systolic thickening of the ischaemic wall remained depressed 4 h after reperfusion and showed some recovery after dopamine infusion. Ischaemic wall stiffness at a common preload was lower after nisoldipine during ischaemia and reperfusion than in controls. Control wall stiffness remained unchanged during the whole experiment with and without nisoldipine. Diastolic thinning of the ischaemic wall was prevented by nisoldipine during ischaemia and after reperfusion. Conclusions: Prolonged myocardial ischaemia is associated with increased myocardial stiffness of the ischaemic wall. Mechanical unloading can help to bridge the acute phase but cannot prevent postischaemic diastolic dysfunction of the ischaemic wall. Nisoldipine has a beneficial effect on regional diastolic function during ischaemia and reperfusion by decreasing regional wall stiffness and preventing diastolic thinning of the ischaemic wall. Cardiovascular Research 1993;27:531-536

In 14 patients (pts) with aortic valve disease (A VD) left ventricular (LV) relaxation was assessed by the time constant (T) of LV pressure (tipmanometer) fall before and 19 months after successful aortic valve replacement (A VR). 12 control pts (CO) were studied by the same technique. Preoperative LV ejection fraction in AVD (64%) and in CO (69%) did not differ. In AVD T was increased (60 ms) as compared to the CO (38 ms, P< 0.05). During handgrip (HG) there was a similar increase of LV peak systolic pressure (LVSP), heart rate and peak measured contractile element velocity of shortening in A VD and in the CO. L V end-diastolic pressure varied minimally in both groups. T decreased during handgrip in CO (38 to 33 ms, P<0.01) and remained unchanged in A VD. Following AVR T at rest decreased insignificantly to 52 ms, but remained increased (P<0.025) as compared with CO. During postoperative HG however, a decrease to 47ms (P<0.05) was noted. Postoperative angiographic LV muscle mass (105 g/m2) and LVSP at rest (137 mmHg) remained elevated (P<0.02) as compared to CO (72 g/m2; 119 mmHg). It is concluded that (1) in A VD with normal ejection performance L V relaxation at rest is prolonged and the reaction of relaxation to HG is abnormal despite preserved contractile response, (2) following A VR the response of LV relaxation to HG becomes normal and (3) elevated postoperative T at rest appears to be related to residual hypertrophy and probably also to the still increased LVSP rather than to intrinsic disturbances of myocardial relaxation

Angiographic techniques have been used for the quantification of mitral or aortic and rarely tricuspid regurgitation. Mitral or aortic regurgitant volume per beat and the regurgitation fraction (fao and fm, respectively) are obtained from the angiographic determination of total left ventricular stroke volume (TSV) and forward stroke volume (FSV) estimated by a different technique. Although this procedure is generally accepted as the gold standard for quantification of left heart regurgitations, there are several limitations: In the presence of mitral and aortic regurgitation no separate quantification of fao and fm is feasible; heart rate at the time of determination of FSV (from Fick or dye dilution cardiac output) and of TSV (angio) may be different; there is a tendency to consistently overestimate stroke volume by angio techniques; repeated estimations of TSV by angio are influenced by the circulatory effects of the contrast dye. In contrast indicator dilution techniques, where upstream and downstream sampling allow the simultaneous estimation of forward and regurgitant flow, the accuracy of the determination of FSV is well established and repeated estimations of fao and fm are possible because the indicators do not have cardiovascular effects. These methods are, however, crucially dependent on thorough mixing of the regurgitant volume with the blood in the upstream chamber. In 23 patients with isolated aortic regurgitation there was a positive correlation between fao evaluated by thermodilution and fao determined by the biplane angio-Fick method (r = 0.59). fao by thermodilution averaged 0.40 and fao by angio-Fick 0.46 (NS). In 23 patients with isolated mitral regurgitation there was also a positive correlation between fm determined by thermodilution and fm determined by angio-Fick (r = 0.71). However, fm by thermodilution was consistently smaller than fm by angio-Fick (average values 0.45 and 0.55, respectively, P < 0.005)

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 <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 under-estimated. 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 is 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

The effect of atrial contraction on cardiac function is reviewed in patients with dual chamber and rate-responsive ventricular pacemakers. The question posed was is there any haemodynamic, clinical or prognostic advantage of AV synchrony in dual chamber pacemakers in comparison to rate-responsive ventricular pacemakers? Optimal A V delay in dual chamber pacing favours cardiac performance at rest, while during exercise the increase in heart rate rather than A V synchrony influences cardiac performance and working capacity. However, there is little information on the benefit of maintained A V synchrony in patients' daily activities. Patients with pacemakers which maintain AV synchrony seem to have less morbidity and mortality than patients with ventricular stimulation alone, and there are comparable rates of complication in carriers of single and dual chamber pacemakers, the former showing problems with the pacemaker syndrome and the latter with atrial sensing and pacemaker-induced tachycardias. The disadvantage of dual chamber pacemakers are higher costs and time-consuming controls

The importance of the right ventricle as a determinant of clinical symptoms, exercise capacity, peri-operative survival and postoperative outcome has been underestimated for a long time. Right ventricular ejection fraction has been used as a measure of right ventricular function but has been found to be dependent on loading conditions, ventricular interaction as well as on myocardial structure. Altered left ventricular function in patients with valvular disease influences right ventricular performance mainly by changes in afterload but also by ventricular interaction. Right ventricular function and regional wall motion can be determined with right ventricular angiography, radionuclide ventriculography, two-dimensional echocardiography or magnetic resonance imaging. However, the complex structure of the right ventricle and its pronounced translational movements render quantification difficult. True regional wall motion analysis is, however, possible with myocardial tagging based on magnetic resonance techniques. With this technique a baso-apical shear motion of the right ventricle was observed which was enhanced in patients with aortic stenosis

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 angioplasly (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 mm after 1·6 mg sublingual nitroglycerin. Workloads before and after PTCA were identical. Percentage diameter stenosis decreased from 78% to 24% (P < 0·001) after PTCA. Mean pulmonary artery pressure increased during exercise from 21 to 40 mmHg (P < 0·001) before and from 19 to 34 mmHg (P < 0·001) after PTCA. Peak exercise pulmonary artery mean pressure was significantly (P < 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 < 0·001) and post- (+31%; P < 0·001) PTCA. In contrast, stenotic vessel segments showed coronary vasoconstriction during exercise before PTCA (−28%; P < 0·01); after PTCA, exercise-induced vasoconstriction of the diseased segment was minimal (−4%; NS). Nitroglycerin was associated with vasodi lation of the stenotic vessel segment before (+17%; NS) as well as after (+26%; P <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. Coronary vasomotion appears to be modified in a positive way by PTCA, but the exact mechanism remains unclear

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 vesorelaxing 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

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 exericse 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<0·001) was found during exercise, whereas the large vessels showed coronary vasodilation (+26%, P<0·001). Coronary flow reserve was significantly (P<0·05) larger in subgroup A (mean 2·5) than in subgroup B (mean 1·2) with exercise-induced vasoconstriction of the small epicardial arteries. In group 2 vasodilation of the normal (+23%, P<0·001) and vasoconstriction of the stenotic coronary arteries (−29, P<0·001) was found during s

Left ventricular (LV) failure can be divided into systolic and diastolic dysfunction. The former is characterized by a reduced ejection fraction and an enlarged LV chamber, the latter by an increased resistance to filling with increased filling pressures. Systolic dysfunction is clinically associated with left ventricular failure in the presence of marked cardiomegaly, while diastolic dysfunction is accompanied by pulmonary congestion together with a normal or only slightly enlarged ventricle. Echocardiography is currently the most relevant technique for non-invasive differentiation of the two forms. Systolic dysfunction is easily assessable by estimation of global ejection fraction and regional wall motion. Diastolic dysfunction can be diagnosed indirectly by means of a normal or nearly normal ejection fraction and changes of the mitral filling pattern in the context of LV failure. For an exact determination of diastolic dysfunction LV catheterization is required. Systolic dysfunction treatment is well defined, consisting of ACE inhibitors, followed by diuretics and digitalis. Calcium channel blockers are usually contraindicated. Diastolic dysfunction therapy is more dependent on the underlying disease. Calcium channel blockers, ACE inhibitors or beta-blockers are first line drugs in most instances: diuretics can be added with increasing symptoms. Digitalis should be avoided, except in atrial fibrillation, to control heart rate

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<0·01) of the normal and coronary vasoconstriction (−29%, P < 0·0·01) of the stenotic vessel segment during bicycle exercise. After sublingual administration of 1·6 mg nitroglycerin there was vasodilation of both normal (+40%, P <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<0·05) and stenotic (+22%, P<0·05) vessel segments showed coronary vasodilation during bicycle exercise. After sublingual nitroglycerin there was further vasodilation of both normal (+31 %, P<0·001 vs rest) and stenotic (+45%, P<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 0·001) and stenotic (−31%, P<0·001) vessel segments. During dynamic exercise there was coronary vasodilation of both vessel segments when compared with 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 with the resting data. After sublingual administration of 1·6mg nitroglycerin both normal (+21%, P−0·01) and stenotic (+36%

In aortic valve stenosis, concentric hypertrophy develops which is characterized by a reduced end-diastolic radius-to-wall thickness ratio (r/h) with an essentially normal cavity shape. As long as the product of (r/h) and LV systolic pressure remains constant, hypertrophy is appropriate. An increase in the product, which represents an increase in wall stress signals inadequate LV hypertrophy. Although at first glance, massive LV hypertrophy appears favourable for the maintenance of a normal LV ejection fraction in aortic stenosis, data from 23 studies of the literature have shown an inverse relationship between ejection fraction and LV angiographic mass m−2 (r=−0·59). Both a degree of hypertrophy inadequate to keep systolic wall stress within normal limits and a reduction of LV contractility may explain the depression of ejection fraction when LV angiographic mass is sizeably increased. Conversely, a normal ejection fraction in aortic stenosis may not be indicative of normal systolic myocardial function under all circumstances. In the presence of mildly reduced contractility, a normal ejection fraction may be maintained by the use of preload reserve. Assessment of myocardial structure from LV endomyocardial biopsies revealed no differences in muscle fibre diameter, interstitial fibrosis and volume fraction of myofibrils between patients with aortic stenosis having a normal and those with a depressed ejection fraction. Preoperative ejection fraction is a poor predictor of postoperative survival, whereas markedly increased preoperative angiographic mass and end-systolic volume have been reported to predict an unsatisfactory postoperative outcome characterized by either death or poor LV function