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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. [ABSTRACT FROM PUBLISHER]

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 nitroglycerin. [ABSTRACT FROM PUBLISHER]

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 action. [ABSTRACT FROM PUBLISHER]

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 exercise. [ABSTRACT FROM PUBLISHER]

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) by angiocardiography and matched with instantaneous volumes obtained by conductivity. There was an excellent correlation between the two techniques at rest (correlation coefficient, = 0.96) and during pressure loading ( = 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 ( <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. [ABSTRACT FROM PUBLISHER]

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. [ABSTRACT FROM PUBLISHER]

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. [ABSTRACT FROM PUBLISHER]

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). [ABSTRACT FROM PUBLISHER]

Left ventricular volumes were determined by means of digital subtraction cineangiocardiography (DSA) which was performed in the right anterior oblique projection after contrast agent injection into the superior vena cava. Monoplane end-diastolic (EDV), end-systolic volumes (ESV), and ejection fraction (EF) were calculated using the ‘area–length’ method and were compared with the same parameters obtained by conventional left ventricular cineangiocardiography. A first group of 20 patients was studied at rest and a second group of 10 patients during bicycle exercise at a work load of 64 watts during 2 min, by DSA and conventional cineangiocardiography. Three different subtraction modes were evaluated: (1) mask mode subtraction (MMS), (2) time interval difference (TID) method and (3) a combination of MMS and TID called MMS+TID method. With the MMS method good correlations were obtained for EDV, ESV and EF at rest (r>0.91) and during exercise (r>0.91). The TID method showed only moderate correlations for patients at rest (r>0.86) and during exercise (r>0.79). Similar results as with MMS were achieved by the combined method (MMS+TID) at rest (r>0.91) and during exercise (r>0.91). Interobserver variability indicated a high reproducibility for all methods except for TID during exercise. It is concluded that DSA is an accurate technique for left ventricular volume determination not only at rest but also during exercise. The best results are obtained with MMS or MMS+TID methods, while left ventricular contour detection is easier and more convenient with MMS+TID. [ABSTRACT FROM PUBLISHER]

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/m) and LVSP at rest (137 mmHg) remained elevated (P<0.02) as compared to CO (72 g/m; 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. [ABSTRACT FROM PUBLISHER]

In patients with hypertrophic cardiomyopathy (HCM), impaired left ventricular (LV) relaxation and diastolic filling have been reported. Therefore, we determined LV diastolic stiffness in nine patients with HCM before and 10 to 15 min after 0·15 mg/kg propranolol i.v. (group 1) and in six patients with HCM before and 10 to 15 min after 0·1 mg/kg verapamil i.v. (group 2). Simultaneous LV cineangiography and high-fidelity pressure measurements were performed in group 1 and simultaneous M-mode echocardiography and high-fidelity pressure measurements in group 2. Passive LV chamber stiffness was determined in group 1 from the diastolic pressure-volume data using an exponential three-parameter model: P =αeβV + C, where P = pressure, α = intercept, β = constant of chamber stiffness, V = volume and C = baseline pressure. Passive LV myocardial stiffness was estimated in group 2 from the diastolic stress-strain data using a viscoelastic model. ο = α′ (eβ′ε - 1) + ηέ, where ο = meridional wall stress, α = intercept, β′ = constant of myocardial stiffness, ε = midwall strain, η = constant of myocardial viscosity and έ = strain rate. LV relaxation was assessed from the time constant of LV pressure decay (T) by plotting LV pressure versus negative dP/dt. LV diastolic filling was evaluated from peak and mean LV filling rate in group I and from peak and mean midwall lengthening rate in group 2.LV chamber and myocardial stiffness, respectively, remained unchanged before and after administration of propranolol (β=0·054 and 0·047) and verapamil (β = 14·8 and 12·6); however, the time constant of LV pressure decay T increased significantly in group I from 45 to 66 ms (P<0·05) and decreased significantly in group 2 from 53 to 43 ms (P<0·05). Parallel to the changes in LV isovolumic relaxation, mean LV diastolic filling rate decreased significantly in group 1 from 257 to 196 ml m−2 s−1 (P<0·025) and mean LV midwall lengthening rate increased significantly in group 2 from 2·37 to 4·31 cm/sec (P<0<05).It is concluded that LV diastolic stiffness remains unchanged in patients with HCM after propranolol and verapamil. LV relaxation and mean diastolic filling, however, are impaired in patients with HCM following propranolol but are improved after verapamil. Thus, the beneficial effect of verapamil on diastolic mechanics is related to improved relaxation and diastolic filling rather than to changes in LV diastolic stiffness. [ABSTRACT FROM PUBLISHER]

Physiologic hypertrophy occurs as the result of exercise conditioning and is characterized by normal or supranormal left ventricular (LV) contractile function and reversibility of structural alterations. Whether hypertrophy produced by chronic abnormal loading can be termed ‘physiologic’ is a matter of debate because in experimental pressure overload hypertrophy normal in vivo ventricular function may be associated with abnormal in vitro function of the papillary muscles. In patients with moderate LV hypertrophy from aortic valve disease (angiographic mass < 180 g/m2) ejection fraction (EF) is preserved, but at similar levels of afterload, when mass exceeds 180 g/m2, EF is depressed. Comparison of LV function with myocardial structure (endomyocardial biopsies) has shown that in patients with compensated LV function and those with left heart failure (EF <57%. LVEDP > 20 mm Hg and/or cardiac index 2·5 l/mm/m2)interstitial fibrosis (IF) was increased to a similar extent (16 and 18%: normal <5%), whereas muscle fiber diameter (MFD normal ≤ 20 μ) was larger (P <0·05) in the patients with failure (30 μ) than in those with preserved function (27 μ). Moreover patients with depressed postoperative function had a larger (P < 001) preoperative MFD (35 μ) than those with normal postoperative function (30 μ). Seventeen months after successful aortic valve replacement IF increased (P < 0·02) and MFD decreased (P < 0·001) but did not become normal regardless whether postoperative function was normal or depressed. Thus in secondary hypertrophy myocardial structure is pathologic even in the presence of normal LV function and depressed function appears likely to be related to excessive fiber hypertrophy rather than to IF. Massive fiber hypertrophy heralds an unfavorable postoperative LV function and fibrosis is irreversible after surgical correction of the abnormal load. [ABSTRACT FROM PUBLISHER]

Five dogs were instrumented with a left ventricular (LV) micromanometer, pairs of ultrasonic crystals to measure L V short axis and L V wall thickness and an inflatable cuff around the ascending aorta. Wall stress, midwall strain and strain rate were calculated at rest, after acute pressure elevation, and one, two and three weeks as well as 24 h after release of aortic constriction. Myocardial wall stiffness and viscosity were determined from a viscoelastic stress-strain model. Reference values at zero pressure were determined in all five dogs. LV end-diastolic pressure increased from 7 mm Hg at rest to 25 mm Hg after acute pressure elevation, to 18 mm Hg after two weeks and decreased to 16 mm Hg after three weeks of pressure elevation, and 11 mm Hg at release of aortic constriction. L V peak systolic pressure increased from 140 mm Hg at rest to 218 mm Hg after acute pressure elevation, to 227 mm Hg after three weeks of pressure elevation and returned to normal (143 mm Hg) after cuff release. Diastolic myocardial wall stiffness showed no change from 23 at rest to 19 after acute pressure elevation, but increased to 47 after one and 81 after two weeks, and it decreased to 50 after three weeks and 45 after cuff release. Myocardial viscosity increased from 0.1 at rest to 3.0 after acute pressure elevation and remained elevated during chronic pressure elevation. The reference values at zero filling pressure showed an increase in LV short axis (creep) from 25.6 mm at rest to a maximum of 28.9 mm after one and two weeks of pressure elevation and then decreased to 27.0 mm after three weeks. LV wall thickness at zero pressure increased from 12.8 mm at rest to 13.7 mm after three weeks of pressure elevation and remained elevated after cuff release (13.8 mm). Thus, diastolic myocardial wall stiffness increased during the initial stages of chronic pressure overload during ventricular dilatation, but decreased when dilatation regressed and concentric hypertrophy developed. Myocardial viscosity was increased during both acute and chronic pressure overload. It is suggested that the early increase in myocardial stiffness may be more importantly related to ventricular dilatation with creep than to wall hypertrophy per se. [ABSTRACT FROM PUBLISHER]

Aims: A simple management strategy is required for patients with acute pulmonary embolism which allows a rapid and reliable diagnosis in order to start timely and appropriate treatment., Methods and Results: Two hundred and four consecutive patients with suspected pulmonary embolism were managed according to a standardized protocol based on the clinical pretest probability and the initial haemodynamic presentation (shock index=heart rate divided by systolic blood pressure). Patients with a high pretest probability and a positive shock index (> or =1) (n=21) underwent urgent transthoracic echocardiography. Based on the presence or absence of right ventricular dysfunction, reperfusion treatment was initiated immediately. Patients with a negative shock index (<1) (n=183) underwent diagnostic evaluation including pretest probability, D-dimer, and spiral computed tomography (CT) as first-line tests. Echocardiography was performed only when a central pulmonary embolism was found in the spiral CT(n=33). According to our strategy, 98 patients met the diagnostic criteria of pulmonary embolism: 75 patients (all shock index <1) were treated with heparin alone, 16 (seven had a shock index > or =1) with thrombolysis, four (all shock index > or =1) with catheter fragmentation, and three (all shock index > or =1) with surgical embolectomy. The all-cause mortality rate at 30 days was 5%, and at 6 months 11%. Right ventricular dysfunction on baseline echocardiography was not associated with a higher mortality rate at 6 months (logrank 2.4, P=0.12)., Conclusions: The novel management strategy for patients with suspected pulmonary embolism resulted in a rapid diagnosis and treatment with a low 30-day mortality. In patients with pulmonary embolism and a positive shock index, time-consuming imaging tests can be avoided to reduce the risk of sudden death and not to delay reperfusion therapy.

Aims: Restenosis after percutaneous coronary angioplasty remains an important limitation of this procedure. This study evaluates whether elevated total plasma homocysteine levels contribute to the development of restenosis after coronary angioplasty., Methods and Results: Two hundred and five patients were recruited after successful angioplasty of at least one coronary stenosis (> or =50%). End-points were restenosis (> or =50%) and a composite of major adverse cardiac events. Of the 205 patients, 183 (89.3%) underwent 6 months angiographic follow-up. Patients with restenosis had significantly higher homocysteine levels than those without (10.9+/- 3.9 micromol x l(-1) vs 9.3+/-3.8 micromol x l(-1), P<0.01). Homocysteine levels were significantly correlated to follow-up diameter stenosis (r=0.24, P=0.0001), especially in small vessels (<3 mm) treated with balloon angioplasty only (r=0.40, P<0.0005). Late lumen loss at follow-up was significantly smaller with homocysteine levels below 9 micromol x l(-1) (0.62+/-0.82 mm vs 0.90+/-0.77 mm, P<0.01). Restenosis rate (25.3% vs 50.0%, P<0.001) and major adverse cardiac events (15.7% vs 28.4%, P<0.05) were also significantly lower in patients with homocysteine levels below 9 micromol x l(-1). Multivariate analysis did not weaken these findings., Conclusion: Total plasma homocysteine is a strong predictor of restenosis and major adverse cardiac events after coronary angioplasty. Thus, plasma homocysteine appears to be an important cardiovascular risk factor influencing outcome after successful coronary angioplasty., (Copyright 2001 The European Society of Cardiology.)

Background: Diastolic dysfunction with delayed relaxation and abnormal passive elastic properties has been described in patients with severe pressure overload hypertrophy. The purpose of this study was to evaluate the time course of rotational motion of the left ventricle in patients with aortic valve stenosis using myocardial tagging., Methods: Myocardial tagging is a non-invasive method based on magnetic resonance which makes it possible to label ('tag') specific myocardial regions. From the motion of the tag's cardiac rotation, radial displacement and translational motion can be determined. In 12 controls and 13 patients with severe aortic valve stenosis systolic and diastolic wall motion was assessed in an apical and basal short axis plane., Results: The normal left ventricle performs a systolic wringing motion around the ventricular long axis with clockwise rotation at the base (-4.4+/-1.6 degrees) and counter-clockwise rotation at the apex (+6.8+/-2.5 degrees) when viewed from the apex. During early diastole an untwisting motion can be observed which precedes diastolic filling. In patients with aortic valve stenosis systolic rotation is reduced at the base (-2.4+/-2.0 degrees; P<0.01) but increased at the apex (+12.0+/-6.0 degrees; P<0.05). Diastolic untwisting is delayed and prolonged with a decrease in normalized rotation velocity (-6.9+/-1.1 s(-1)) when compared to controls (-10.7+/-2.2 s(-1); P<0.001). Maximal systolic torsion is 8.0+/-2.1 degrees in controls and 14.1+/-6.4 degrees (P<0.01) in patients with aortic valve stenosis., Conclusions: Left ventricular pressure overload hypertrophy is associated with a reduction in basal and an increase in apical rotation resulting in increased torsion of the ventricle. Diastolic untwisting is delayed and prolonged. This may explain the occurrence of diastolic dysfunction in patients with severe pressure overload hypertrophy.

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 greater than or equal to 0.80; method 2, r greater than or equal to 0.75). The standard error of estimate of the mean (SEE) was slightly lower for method 2 (less than or equal to 10%) than for method 1 (less than or equal to 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 less than or equal to 15% for method 1 and less than or equal to 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 overestimated and with method 2 underestimated.