Dynamics of aortic flow in hypertrophic cardiomyopathy

The purpose of this study was to reassess left ventricular ejection dynamics in hypertrophic cardiomyopathy, to investigate whether a premature stoppage of ejection occurs, as previously reported, and whether reliable criteria for left ventricular outflow tract obstruction can be established by non-invasive evaluation of aortic flow patterns. In a group of 21 patients with hypertrophic cardiomyopathy, composed of 9 with the obstructive form (HOCM), 9 with the non-obstructive form (HNCM) and 3 with apical hypertrophy (HACM), instantaneous flow velocities across the ascending aorta were determined non-invasively with a 16-gated Doppler 2-D echo instrument. Ten normals served as controls. The 16 flow velocities were averaged over 8 heart beats and the relative volume flow rate was calculated by microprocessor analysis. Ejection time (i.e. flow time) derived from the flow curves was compared with the available ejection period as determined from the carotid pulse tracing. In normals, ejection time amounted to 94±3% of the available ejection period, in HOCM to 92±5% and in HNCM to 93±4% (no significant differences). In HACM, however, ejection time was reduced to 71±14% of the available ejection period. In contrast to HNCM, aortic flow in HOCM was characterized by an early peak followed by a plateau at a sizeably lower flow level for the rest of systole. Flow time of an abnormally short duration was the hallmark of HACM. We conclude that in patients with hypertrophic cardiomyopathy, HOCM and HNCM can be distinguished by the shape of their volume flow curves. A premature stoppage of ejection is only found in patients with HAC

Estimation of left ventricular volume from apical orthogonal 2-D echocardiograma

In 42 consecutive patients undergoing biplane left ventricular cine-angiography, left ventricular volumes were first determined ultrasonically using a phased array transducer. To this end, two orthogonal apical long axis views were recorded one illustrating all four chambers, the other being the ‘RA O equivalent' view. Left ventricular volumes wer estimated by applying the area-length method to both two-dimensional echocardiograms and cine-angiograms, consistently including in the former the left ventricular outflow tract of the ‘RAO equivalent' view. The echocardiographic approach employed was shown to yield good predictions of the angiographic results. For the end-diastolic volume the correlation is characterized by r=0.98 and SEE 21 ml or 9.7% of the angiographic mean and for the end-systolic volume by r=0.97 and SEE 17 ml or 18.1% of the mean. The correlation for the ejection fraction showed an r value of 0.87 and a SEE of 5.4%. Equally good correlations were obtained in the subgroup with wall motion disorders for which the r values of the end-diastolic and end-systolic volumes were both 0.98 and that of the ejection fraction was 0.8

A comparison between single gate and multigate ultrasonic Doppler measurements for the assessment of the velocity pattern in the human ascending aorta

The velocity pattern in the ascending aorta of 15 healthy adults was measured quasisimultaneously from the Doppler-shifts produced in 16 gates distributed equally within the cross-section along a narrow ultrasound beam which centrally traversed the vessel upstream of the brachiocephalic trunk. A comparison between the time integrals of the velocities in gates 9 (centre line), 4 and 13 (off centre) and the time integral of the weighted mean of the velocities of all gates correlated with r=0.90, SEE=1.05 (gate 9), r=0.90, SEE 0.88 (gate 4) and r=0.92, SEE 0.94 (gate 13). A better correlation (r=0.96, SEE=0.60) was found between the linear mean of all gates and the weighted mean. These results show that Doppler measurements in single small gates are not appropriate to determine the average cross-sectional blood flow velocity in healthy adult

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<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%, P<0·001) vessel segments showed coronary vasodilation. It is concluded that supine bicycle exercise in patients with coronary artery disease is associated with vasodilation of the normal and vasoconstriction of the stenotic coronary arteries. Intravenous administration of propranolol is followed by coronary vasoconstriction of both normal and stenotic coronary arteries, probably due to secondary mechanisms because it is not observed after intracoronary injection of propranolol and it is overridden by bicycle exercise and sublingual nitroglyceri

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<0·01) and after sublingual administration of nitroglycerin (+40%, P<0·001). In group 2 luminal area increased after intracoronary administration of diltiazem (+19%, P<0·01), during bicycle exercise (+23%, P<0·001) and after sublingual administration of nitroglycerin (+39%, P<0·001). Stenotic vessel: In the control group luminal area decreased significantly (−29%, P<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<0·05). There was a further increase in stenosis area during bicycle exercise (+23%, P<0·001 vs. rest) and after sublingual nitroglycerin (+32%, P<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<0·05). Thus, it is concluded that diltiazem prevents exercise-induced coronary vasoconstriction of the stenotic vessel segment probably due to its direct vasorelaxing action on the smooth vasculature. Diltiazem combined with nitroglycerin elicits an additive effect on coronary vasodilation of the stenotic vessel segments but not on the normal coronary arteries. The exact mechanism of this additive effect is not clear but might be due to the combined action of the two vasoactive drugs with different mode of actio

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 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 unclea

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 <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 intervention

Fluorescence spectroscopy for identification of atherosclerotic tissue

Objective: Vessel perforation and limited steerability of the laser light are the major limitations of laser angioplasty. To improve steerability fluoresence spectroscopy has been proposed for identification of atherosclerotic plaques. The aim was to investigate this. Methods: Fluorescence spectroscopy with three different excitation wavelengths (325 nm, 380 nm, 450 nm) was tested in an emission range of 400 nm to 600 nm. Intensity ratios at 480/420 nm were determined in different types of blood vessels. Necropsy material from 40 patients (punch biopsies of 4 mm diameter from the coronary and carotid artery as well as from the ascending and descending aorta) was studied spectroscopically. Histological alterations of the vessel wall were assessed by a semiquantitative score (0 to 10 points): (a) normal tissue, 0 to 2 points (mean=0.25; n=38); (b) mild atherosclerotic lesions, 3 to 5 points (mean=3.35; n=39); (c) severe atherosclerotic lesions, ≥ 6 points (mean=6.75; n=43). Results: Best spectroscopic results were obtained with an excitation wavelength of 325 nm. In samples with severe atherosclerotic lesions the fluoresence spectra showed a significant reduction of the emitted wavelength intensities when compared to normal tissue. There was a clear separation of the fluorescence spectra between normal and mild as well as between normal and severe atherosclerotic lesions; normal tissue showed an increased intensity in the range from 420 nm to 540 nm, whereas atherosclerotic lesions had no or only a small peak at 480 nm. There was a significant correlation between the semiquantitative score (n=120) and the fluorescence ratio at 480/420 nm (excitation wavelength 325 nm) with a correlation coefficient of 0.87. The spectroscopic results showed no differences between the samples taken from different types of vessels. Conclusions: Fluorescence spectroscopy allows a reliable identification of normal and atherosclerotic lesions. The close correlation between the emitted light intensity ratio at 480/420 nm and the histological alterations of the vessel wall suggests a relationship between vessel wall fluorescence and the atherosclerotic alterations of the wal

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 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 supine bicycle exercise. Administration of sublingual nitroglycerin at the end of the exercise test was accompanied by coronary vasodilation of both normal (+40%, P<0·001 vs rest) and stenotic (+12%, NS vs rest) vessel segments. It is concluded that isometric exercise is associated with reflex coronary vasoconstriction of the normal and stenotic vessel segments due to enhanced sympathetic stimulation. Dynamic exercise in patients with ischaemia-like symptoms and normal coronary arteries is accompanied by an abnormal dilatory response of the small coronary arteries in a subgroup of patients with reduced coronary flow reserve. Dynamic exercise in patients with coronary artery disease is, however, associated with coronary vasodilation of the normal and coronary vasoconstriction of the stenotic vessel segments. The nature of this exercise-induced vasoconstriction of stenotic coronary arteries is not clear, but might be related to endothelial dysfunction with an insufficient production of the endothelium-derived relaxing factor during exercis

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<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 reserv