Results and indications of coronarography in mitral valvulopathies

Selective coronary angiography was carried out in 110 patients (68 women, 42 men; average age 57 +/- 8 years) with significant, isolated, non-ischaemic mitral valve disease. The indication for coronary angiography was angina or myocardial infarction in 42 cases and the investigation was carried out routinely in the other 68 cases. Coronary stenosis greater than 50 p. 100 was demonstrated in 25 cases (22.7 p. 100), 18 single vessel, 5 double or triple vessel disease and 2 cases of stenosis of the left main stem. The incidence of coronary artery disease was higher in patients with cardiovascular risk factors (0 factors: 13 p. 100; 1 factor: 22 p. 100, 2 or 3 factors: 45 p. 100; p less than 0.01). The coronary patients had higher mean pulmonary artery pressures (33 +/- 16 mmHg vs 25 +/- 8 mmHg, p 0.001), higher left ventricular end diastolic pressures (12.5 +/- 7 mmHg vs 9 +/- 5 mmHg, p less than 0.01) and greater left ventricular end diastolic volumes (83 + 40 ml/m2 vd 59 +/- 29 ml/m2, p less than 0.01). There was no difference in segmental wall motion between coronary and non coronary patients. 89 patients were referred for surgery, 17 of whom had coronary artery disease. 5 patients underwent coronary bypass surgery. The incidence of peroperative cardiac complications (low output, ventricular arrhythmias, myocardial infarction) was higher in the coronary patients (53 p. 100 vs 18 p. 100, p less than 0.01). The 6 year survival rate was 75 +/- 8 p. 100.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alterations in myocardial metabolism and function at rest in stable angina pectoris: relations with the amount of exercise-induced thallium-201 perfusion defect

The relation between the amount of exercise-induced ischemia and alterations in left ventricular (LV) function and metabolism at rest was studied in 18 coronary patients with stable angina pectoris. An ischemic defect area score was computed from quantitative exercise thallium-201 (Tl-201) scintigraphy; this estimation of the amount of ischemic myocardium was used to classify the patients in group I (n = 8; score less than 15%, mean 6.7 +/- 2.5%) and II (n = 10; score greater than 15%; mean 27.2 +/- 8.9%). Hemodynamics and metabolism were studied in basal state. No patient had anginal pain during the study, and the extent of angiographic coronary artery disease (CAD) was comparable in the two groups. Heart rate, aortic pressure, coronary blood flow, and myocardial oxygen uptake were also similar in both groups. However, ejection fraction was reduced in group II (51 +/- 13 vs 63 +/- 5%; p less than 0.01) and LV relaxation was impaired as shown by the increase in time-constant of isovolumic pressure fall (55 +/- 16 vs 44 +/- 6 ms in group I; p less than 0.05); the LV end-diastolic pressure was also increased in group II (19 +/- 8 vs 10 +/- 4 mmHg in group l; p less than 0.05). Furthermore, in group II, myocardial lactate uptake was reduced (4 +/- 19 vs 30 +/- 29 mumole/min in group I; p less than 0.01) and the productions of alanine and glutamine were augmented (-7.5 +/- 4.4 vs -4.6 +/- 1.6 mumole/min in group I; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

ST segment response to acute coronary occlusion: coronary hemodynamic and angiographic determinants of direction of ST segment shift

To assess the relationship between the direction of ST segment response to transient coronary occlusion and collateral function, we studied 25 patients with diagnostic ST segment changes during transient occlusion of the proximal left anterior descending artery (LAD). Electrocardiographic leads I, II, V2, and V5; left ventricular filling, aortic, and distal coronary pressures; and great cardiac vein flow were measured during percutaneous transluminal coronary angioplasty (PTCA) of the LAD. During a 1 min LAD balloon occlusion, 16 patients had reversible ST elevation (group I) and nine patients had ST depression (group II). The ST responses in individual patients were consistent during repeated occlusions, and ST depression never preceded ST elevation. Angiography before PTCA showed less severe LAD stenosis in group I (69 +/- 15%) than in group II (88 +/- 10%; p less than .01) and collateral filling of the LAD in no group I patient but in six of nine patients in group II (p less than .01). During LAD occlusion, determinants of myocardial oxygen demand (left ventricular filling pressure, aortic pressure, heart rate, and double product) were similar in both groups. Group I patients, however, had lower distal coronary pressure (25 +/- 8 vs 41 +/- 16 mm Hg) and residual great cardiac vein flow (33 +/- 14 vs 51 +/- 22 ml/min) and higher coronary collateral resistance (3.1 +/- 2.1 vs 1.5 +/- 0.8 mm Hg/ml/min) than group II patients (all p less than .05). In patients with ST elevation during LAD occlusion, stenosis before PTCA was less severe, visible collaterals were not present, and hemodynamic variables during LAD occlusion reflected poorer collateral function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of intracoronary fibrinolysis and conventional treatment of myocardial infarction

57 patients with a complete coronary thrombosis were treated by intracoronary fibrinolysis during the first 6 hours of inaugural myocardial infarction. The artery was revascularised in 37 cases (65 p. 100). Eleven patients had isolated stenosis of the left anterior descending artery and 16 patients isolated stenosis of the right coronary artery. These patients were compared with 27 other patients admitted between the 6th and 18th hours of primary myocardial infarction treated conventionally, in whom coronary angiography performed between the 14th and 21st day after infarction showed isolated left anterior descending disease in 14 cases (9 thromboses and 5 stenoses) and isolated right coronary disease in 13 cases (7 thromboses and 6 stenoses). The haemodynamic data and heart rates were identical in both groups during control coronary angiography between the 14th and the 21st days. Global left ventricular function and regional wall motion were studied by 30 degrees right anterior oblique ventriculography using the Stanford method before fibrinolysis in the first group and at the end of the 3rd week in both groups. In LAD, repermeabilisation by fibrinolysis, significant improvements were observed in ejection fraction (EF p. 100 = 42 +/- 9 vs 50.6 +/- 14 p. 100, p less than 0.05); fractional shortening of the hypokinetic segment (FS p. 100 = 4.5 +/- 4.6 vs 12.4 +/- 8.8 p. 100, p less than 0.001), and in the number of hypokinetic or akinetic segments (6.0 +/- 1.1 vs 4.2 +/- 2.1, p less than 0.05). Segmental and global left ventricular function was much poorer in the group treated conventionally at the 21st day (EF p. 100 = 44 +/- 11 p. 100, p less than 0.05; FS p.t100 = 5.8 +/- 9.7 p.t100, p less than 0.05; number of diseased segments: 6.0 +/- 1.4, p less than 0.01). On the other hand, the improvement was less marked in patients with inferior wall infarction; the results in the two groups were comparable.     

Clinical study of late potentials--comparison of late potentials in myocardial infarction, cardiomyopathy and idiopathic ventricular tachycardia

Late potentials (LPs) were studied using the signal averaging technique in 80 patients with myocardial infarction (MI), idiopathic cardiomyopathy (CM) and idiopathic ventricular tachycardia (IVT). In MI, LP duration was 28.4 +/- 12.6 ms in the sustained VT group (I; 8 cases); 18.6 +/- 9.0 ms in the non-sustained VT group (II; 11 cases); and 14.4 +/- 8.6 ms in the non-VT group (III; 21 cases); (p less than 0.05 in I vs II, p less than 0.01 in I vs III and not significant in II vs III). In CM, it was 33.7 +/- 13.0 ms in group I (6 cases); 20.1 +/- 5.9 ms in group II (12 cases); and 7.1 +/- 9.2 ms in group III (14 cases); (p less than 0.01 in I vs II, I vs III and II vs III). The LP duration in IVT (8 cases) was 15.6 +/- 10.4 ms, which was significantly shorter than that of group I in MI and CM (p less than 0.05 vs MI and p less than 0.01 vs CM). Late potential duration was also compared between a pacing-inducible VT group and a non-inducible VT group. The mean value of LP duration in the inducible VT group of MI was significantly longer than that in the non-inducible group (27.8 +/- 3.9 ms in 4 cases vs 17.3 +/- 2.5 ms in 4 cases, p less than 0.05). However, there was no significant difference in LP duration between the inducible and non-inducible groups of CM (22.0 +/- 11.0 ms in 5 cases vs 22.2 +/- 13.6 ms in 5 cases).(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary flow studies in patients with left ventricular hypertrophy of the hypertensive type. Evidence for an impaired coronary vascular reserve

Increased myocardial blood flow occurs in ventricular hypertrophy, but flow per 100 grams of myocardium remains normal. The increase in flow may be obtained at the expense of the existing coronary vascular reserve or by an increase in the vascular bed. The coronary vascular reserve was studied by analyzing the hyperemic reaction to selective injection of contrast agent into the coronary arteries in 25 patients: a control group (9 patients) with chest pain syndrome, normal coronary arteries and a normal left ventricle (Group I) and 16 patients with aortic stenosis, left ventricular hypertrophy and normal coronary arteries (Group II). The hyperemic response in Groups I and II was 73.3 +/- 2.2 and 65.8 +/- 9.1 percent, respectively (difference not significant). Group II was subdivided into two groups: Group IIA had five patients with a left ventricular mass of less than 200 g (mean 158.8 +/- 25.9); this group had a hyperemic response of 102.3 +/- 9.9 percent. Group IIB had 11 patients with a left ventricular mass of more than 200 g (mean 308.9 +/- 22.5) and a hyperemic response of 49.27 +/- 10.42 percent. The hyperemic response was correlated with the diastolic left ventricular-aortic gradient (r = +0.64, p less than 0.001), left ventricular mass (r = -0.51, p less than 0.01) and aortic diastolic pressure (r = +0.636, p less than 0.001). Group I had a left ventricular mass similar to that of Group IIA (124.9 +/- 9 and 158.8 +/- 26 g, respectively) but a lower hyperemic response (73.3 +/- 2 and 102.3 +/- 10 percent, respectively). These data suggest that severe left ventricular hypertrophy is associated with a reduction in coronary vascular reserve; it is speculated that this decrease in the vascular reserve capacity may be related to the ischemic component of hypertrophic heart disease.     

Early changes in ventricular function in diastolic phase in the resting coronary patient

The aim of this study is to test left ventricular diastolic function in coronary artery disease patients with preserved systolic performance. Two groups of patients (25 coronary artery disease patients with angiographic proved coronary artery stenosis, but with normal hemodynamic and angiographic indices of systolic phase, first group; and 14 normal subjects for control, second group) were tested comparing their systolic and diastolic ventricular function indices, obtained by using a Millar microtip catheter and a computerized program. Systolic ventricular function was similar in the two groups (EF: 0.61 +/- 0.05 vs 0.62 +/- 0.03, p: n.s.; Vmax:120 +/- 28 vs 112 +/- 24 sec-1, p: n.s.), while diastolic indices were significantly different (lowest diastolic pressure: 3.7 +/- 2.4 vs -1.72 +/- 1.45 mmHg, p less than 0.01; end-diastolic pressure: 11.2 +/- 4.2 vs 6.5 +/- 2.8 mmHg, p less than 0.05; T constant: 45 +/- 8 vs 35 +/- 6 mmHg, p less than 0.001; end-diastolic compliance: 2.79 +/- 0.3 X 10(-2) vs 5.68 +/- 0.4 X 10(-2) mmHg-1, p less than 0.001; Kp: 0.041 +/- 0.006 vs 0.003 +/- 0.004 p less than 0.001). In conclusion, impairment of left ventricular diastolic phase may be one of the earliest manifestations of functional alterations of ischemic ventricle.     

Interventricular delay in severe aortic stenosis recognized by gated radionuclear blood pool scanning

Twenty-four patients referred for cardiac catheterization for suspected aortic stenosis were investigated by equilibrium gated blood pool study. From the time-activity curves, end systole for each ventricle was determined and the delay between the two was calculated. The patients were divided into three groups according to their calculated aortic valve area. The mean delay in a control group of 20 normal subjects was 6 +/- 13 msec (mean +/- standard deviation). In group I (aortic valve area greater than 0.75 cm2) the delay was 16 +/- 25 msec (p = NS compared to controls); in group II (aortic valve area 0.5 to 0.75 cm2) the delay was 28 +/- 27 msec (p less than 0.01); and in group III (aortic valve area less than 0.5 cm2) the delay was 60 +/- 28 msec (p less than 0.001). Ten patients were restudied after valve replacement; their mean delay decreased markedly from 48 +/- 19 to 5 +/- 26 msec (p less than 0.001). Thus, this method appears to identify patients with severe aortic stenosis and may therefore be a useful adjunct to the noninvasive assessment of this disorder both before and after surgery.     

Higher Gensini score of coronary arteries in acute inferior myocardial infarction with precordial ST-segment depression.

To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (greater than or equal to 1 mm in V2-V6) and Group II (n = 16) those without ST-segment depression (less than 1 mm). The Gensini score of the coronary arteries (56 +/- 29 vs. 28 +/- 18; p less than 0.001), the partial score of the infarction-related artery (29 +/- 16 vs. 17 +/- 11; p less than 0.01) and of the infarction-nonrelated artery (27 +/- 24 vs. 11 +/- 12; p less than 0.02) were significantly higher in Group I than in Group II. The Killip score (greater than or equal to II) (34% vs. 6%; p less than 0.05), frequency of arrhythmias (75% vs. 38%; p less than 0.02) and peak CK value (3,676 +/- 2,290 vs. 1,818 +/- 1,153 IU/L; p less than 0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms. All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8 +/- 19.6 cm2 in Group I (n = 14) and 34.7 +/- 21.3 cm2 in Group II (n = 8; N.S.). In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.     

Right ventricular function during the convalescence phase of posterior primary infarction

Right ventricular extension is very common in inferior myocardial infarction and the resulting haemodynamic changes are well documented. The aim of this prospective study was to assess the consequences on regional and global right ventricular function at a distance from the initial episode. The study population included 32 patients (29 men and 3 women; mean age 52.7 +/- 6 years) admitted consecutively to the coronary care unit for acute inferior wall myocardial infarction with right ventricular extension (group A: 14 patients) or without (group B: 18 patients), based on the initial haemodynamic data. All patients underwent right and left cardiac catheterisation with selective biplane right and left ventriculography and coronary angiography, 2.9 +/- 1 months after the acute episode. In group A, there was a normalisation of the haemodynamic changes observed during the acute phase of myocardial infarction, complete occlusion (10 cases) or a significant residual stenosis (3 cases) of the right coronary artery proximal or immediately distal to the right marginal artery and persistence of an alteration of global right ventricular systolic function when compared with group B (increased end systolic volume: RVESV = 43 +/- 11 ml/m2 vs 35 +/- 9 ml/m2, p less than 0.02, and a decreased ejection fraction: RVEF = 49 +/- 7 p. 100 vs 57 +/- 9 p. 100, p less than 0.01, resulting from hypokinesia or akinesia of the right ventricular inferior wall; mean shortening delta R = 11 +/- 6 p. 100 vs 17 +/- 7 p. 100, p less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)     

Regression of residual coronary stenosis after recanalization by fibrinolysis in myocardial infarction. Quantitative analysis of coronary angiography immediately after obstruction removal, at a 15-day and 3-month follow-up

There seems to be a high risk of reobstruction after local fibrinolytic therapy in myocardial infarction because the severity of the residual stenosis. However, it is quite common to observe a significant improvement of these stenoses at follow-up coronary angiography. Also, one may demonstrate a patent coronary artery after initial failure of the recanalisation procedure. The aim of this research was to study objectively the outcome of the residual coronary stenosis after intracoronary fibrinolytic therapy during myocardial infarction. The degree of stenosis expressed as a percentage reduction of the average diameter of the vessel measured in two perpendicular incidences was assessed immediately after initial fibrinolytic therapy, and at 15 days and 3 months' follow-up. The study group of 31 patients was divided into two subgroups: group I (16 patients) with successful revascularisation and a patent vessel at the first control; and group II (15 patients): unsuccessful revascularisation or with reobstruction at the first control angiography (2 cases). The coronary angiographies were interpreted by an observer who had no knowledge of the patients or of the order of the investigations. In group I, the degree of stenosis decreased from 74 +/- 18 p. 100 to 64 +/- 16 p. 100 (p less than 0.05) at the first control, and then to 47 +/- 24 p. 100 (p less than 0.001) at the second control (less than 50 p. 100 in 7 cases).(ABSTRACT TRUNCATED AT 250 WORDS)     

Aortic valve sclerosis is associated with systemic endothelial dysfunction

OBJECTIVES: We sought to examine the association between aortic valve sclerosis (AVS) and systemic endothelial manifestations of the atherosclerotic process. BACKGROUND: Clinical and experimental studies suggest that AVS is a manifestation of the atherosclerotic process. Systemic endothelial dysfunction is an early sign of the atherosclerotic process and can be assessed by ultrasonography of the brachial artery. METHODS: A total of 102 in-hospital patients (76 men; mean age 63.5 +/- 9.7 years) referred to the stress echocardiography laboratory underwent: 1) transthoracic echocardiography, with specific assessment of AVS (thickened valve leaflets with a transaortic flow velocity <2.5 m/s); 2) stress echocardiography; 3) coronary angiography, with evaluation of the Duke score (from 0 [normal] to 100 [most severe disease]); and 4) an endothelial function study, with assessment of endothelium-dependent, post-ischemic, flow-mediated dilation (FMD). RESULTS: Aortic valve sclerosis was present in 35 patients (group I) and absent in 67 (group II). Groups I and II were similar in terms of the frequency of stress-induced wall motion abnormalities (35.3% vs. 19.4%, p = NS) and the angiographic Duke score (33.8 +/- 28.6 vs. 35.2 +/- 29.1, p = NS). Patients with AVS showed a markedly lower FMD than those without AVS (2.2 +/- 3.5% vs. 5.3 +/- 5.3%, p < 0.01). On multivariate analysis, only FMD was highly predictive of AVS, with an odds ratio of 1.18 for each percent decrease in FMD (95% confidence interval 1.05 to 1.32; p = 0.01). CONCLUSIONS: Aortic valve stenosis is associated with systemic endothelial dysfunction. This observation may provide a mechanistic insight into the emerging association between AVS and cardiovascular events.     

Anterior lead ST-segment depression in inferior wall infarction. Early angiographic study. Effect on the results of intracoronary thrombolysis

Of 32 patients with inferior myocardial infarction undergoing coronary angiography in the first 6 hours for intracoronary streptokinase thrombolysis, 19 (Group I) had ST depression of more than 1 mm in the anterior chest wall leads (VI-V4) whilst 13 (Group II) had no ST changes in these leads. Quantitative analysis of left ventricular angiograph showed a significantly lower ejection fraction in Group I (52 +/- 8.5%) compared to Group II (59 +/- 8%, p less than 0.05) and that this difference was due to a greater zone of inferior wall hypokinesia, irrespective of whether this was assessed by measuring its surface area (HKS cm2: Gr I: 11 +/- 6, Gr II: 4 +/- 3, p less than 0.01) or percentage ventricular perimeter (HK%: Group I 45 +/- 15, Group II 26 +/- 12, p less than 0.001). On the other hand, anterior wall motion was normal in both groups. Coronary angiography showed proximal obstruction of the right coronary artery in 84% of patients in Group I. In Group II, the coronary obstruction tended to be distal or incomplete. The prevalence and average severity of associated stenosis of the left anterior descending artery were the same in both populations. The success rate of thrombolysis was not significantly different between the two groups. In successful procedures with a patent artery on the 14th day, improved regional contractility was only observed in Group I (HKS cm2: 11.5 +/- 6 vs 8 less than 4.4, p less than 0.05; HK%: 47 +/- 14 vs 38 +/- 9, p less than 0.05): the hypokinetic zone was unchanged in Group II.(ABSTRACT TRUNCATED AT 250 WORDS)     

ST segment shift in unstable angina: pathophysiology and association with coronary anatomy and hospital outcome

The significance of ST segment shift with respect to coronary anatomy and hospital outcome was evaluated in 135 patients with unstable angina. ST shift was evident in 44% of patients on admission electrocardiogram (ECG) and in 66% on Holter monitor ECG. During hospitalization, 7% of patients had myocardial infarction, 4% died and 34% had urgent coronary revascularization. By comparing patients with and without ST shift on admission ECG, an unfavorable outcome was found in 55% versus 25% (p less than 0.005), multivessel disease in 77% versus 63% (p less than 0.05) and left main coronary artery stenosis in 22% versus 7% (p less than 0.025). When patients with and without ST shift on Holter monitor ECG were compared, an unfavorable outcome was found in 48% versus 20% (p less than 0.005), multivessel disease in 76% versus 54% (p less than 0.01) and left main coronary stenosis in 18% versus 4% (p less than 0.05). The duration of ST shift was also greater in patients with 1) unfavorable outcome (129 +/- 136 versus 52 +/- 111 min, p less than 0.01); 2) multivessel disease (98 +/- 129 versus 36 +/- 90 min, p less than 0.01); and 3) left main stenosis (150 +/- 147 versus 67 +/- 114 min, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Determination of the size of the right atrium in patients with pulmonary hypertension using 2-dimensional echocardiography

Normal values for right atrial area and tricuspid annular diameter and their percentage shortening measured from the two-dimensional echocardiographic four-chamber view are now available. In this study right atrial size of patients with pulmonary hypertension is evaluated and the results compared with the M-mode findings of the right ventricle in order to detect pulmonary hypertension. Hemodynamics and echocardiograms of 60 patients (mean age 57 +/- 10 years) with mitral stenosis III-IV NYHA and concomitant pulmonary hypertension were examined. 20 patients in group I with atrial fibrillation had additional functional tricuspid incompetence. Unlike the 20 patients in group II, who had atrial fibrillation, the remaining 20 in group III were still in sinus rhythm. The mean pulmonary artery pressure was 44.1 +/- 9.3 mmHg in group I, in group II 33.9 +/- 6.3 mmHg (grp. I vs. grp. II p less than 0.001) and in group III 33.2 +/- 7.1 mmHg (grp. II vs. grp. III ns). The end-systolic index of the right atrial area in group I was 19.6 +/- 5.7 cm2/m2 and thus significantly greater than in group II with 10.6 +/- 2.3 cm2/m2 (p less than 0.001) and in group III with 9.1 +/- 2.5 cm2/m2 (p less than 0.001). The maximal diameter of the tricuspid annulus measured 24.6 +/- 5.5 mm/m2 in group I, 18.9 +/- 3.5 mm/m2 in group II (grp. I vs. grp. II p less than 0.001) and 20.2 +/- 2.2 mm/m2 in group II (grp. I vs. grp. II p less than 0.001) and 20.2 +/- 2.2 mm/m2 in group III.(ABSTRACT TRUNCATED AT 250 WORDS)     

Results of balloon aortic valvuloplasty in patients with aortic stenosis associated with significant aortic regurgitation

The influence of balloon aortic valvuloplasty (BAV) on aortic regurgitation (AR) in patients with severe aortic stenosis associated with greater than or equal to grade II AR was studied by supraaortic angiogram before and after BAV. The results of 50 patients aged 72 +/- 12 years with significant AR before BAV (group A) were compared to 297 patients (mean age 76 +/- 10 years) with no or mild AR (group B). In group A, the patients had a higher left ventricular end diastolic volume (96 +/- 19 mL/m 2 vs 81 +/- 32 mL/m 2, P less than 0.01) and left ventricular end diastolic pressure (23 +/- 9 mmHg vs 19 +/- 9 mmHg, P less than 0.01). The aortic valve area was similar in both groups. Following BAV, the improvement in aortic valve area and hemodynamics were similar in both groups. In group A, AR remained unchanged in 31 patients (62%), increased by 1 grade in 13 patients (26%), and decreased by 1 grade in 6 patients (12%). In group B, AR increased by greater than 1 grade in 34 patients (11%) and greater than 2 grades in 4 patients (1.3%) post-BAV. Two patients in group B underwent emergency aortic valve replacement following BAV because of severe acute AR. In conclusion, when it is indicated, BAV can be performed with similar risk in patients with significant AR.     

Frequency of low-grade residual coronary stenosis after thrombolysis during acute myocardial infarction

The clinical, angiographic and demographic characteristics of 42 patients with low-grade (less than 50%) residual stenosis at the infarct lesion after thrombolysis for acute myocardial infarction (MI) were assessed. The study group (group I) represented 21% of 198 consecutive patients receiving thrombolytic therapy over a 59-month period. Data on the 156 remaining patients were pooled for comparison (group II). Group I patients were predominantly men (86%) who were cigarette smokers (81%). Group II patients were predominantly men (75%, p greater than 0.10) but were significantly older (52 +/- 12 vs 56 +/- 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (greater than 50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (greater than 50% diameter stenosis) residual vessel disease was 0.6 +/- 1.0 for group I and 1.9 +/- 0.9 for group II (p less than 0.001). In group I, average residual infarct lesion diameter stenosis was 36 +/- 7% in the right anterior oblique and 34 +/- 8% in the left anterior oblique views. Thirty-nine group I patients were discharged with medical therapy and 100% follow-up was obtained over a mean interval of 18 +/- 17 months. Fifteen patients experienced chest pain after acute MI accounting for 17 discrete events. Fifty-nine percent of group I had a benign course on follow-up. Eight events were classified as unstable angina, 4 as acute MI and 5 as atypical angina. Documented coronary vasospasm occurred in 3.(ABSTRACT TRUNCATED AT 250 WORDS)     

Midterm outcome of patients with asymptomatic restenosis after coronary balloon angioplasty.

Although many patients with restenosis after balloon coronary angioplasty have recurrence of angina, others remain asymptomatic. To assess the clinical implications of asymptomatic coronary restenosis, we analyzed clinical and angiographic characteristics of 277 consecutive patients with restenosis, 133 (48%) of whom were asymptomatic (group I) and 144 (52%) symptomatic (group II). Restenosis was documented 6 to 9 months after the index procedure, or earlier if angina recurred, and was defined as a greater than 50% lumen narrowing (visual estimation). Group I (asymptomatic group) included fewer female (9% vs. 18%, p less than 0.05) and hypertensive patients (38% vs. 56%, p less than 0.005) and more patients with a previous myocardial infarction (48% vs. 28%, p less than 0.05) and single-vessel disease (67% vs. 55%, p less than 0.05). Before angioplasty, symptoms had lasted for a shorter period (10 +/- 25 vs. 23 +/- 42 months, p less than 0.001), ischemia after a recent infarction was a more frequent indication (21% vs. 10%, p less than 0.05) and total revascularization more frequently obtained (74% vs. 63%, p less than 0.05) in group I than in group II patients. Only a normal blood pressure, previous myocardial infarction, single-vessel disease and a shorter duration of symptoms were independent correlates of asymptomatic restenosis. No differences were found in stenosis severity before angioplasty (90% in both groups) or after angioplasty (22% +/- 12% vs. 24% +/- 16%).(ABSTRACT TRUNCATED AT 250 WORDS)     

The local and systemic effects of intracoronary ergonovine in patients with normal and nonspastic coronary arteries. A comparison with the intravenous ergonovine test

Local and systemic effects of intracoronary (two bolus injections of 25 micrograms at 3-min intervals) ergonovine were determined in 60 patients with angiographic non-spastic normal coronary arteries and were compared with the most usual intravenous ergonovine dose to induce coronary artery spasm (incremental doses of 50, 100 and 200 micrograms at 3-min intervals). The mean diameter of the vessels was reduced by 15% after selective injections (baseline 2.38 +/- 0.7; after intracoronary ergonovine 2.02 +/- 0.6 mm; p less than 0.001) and no significant changes were induced in the heart rate (before 80 +/- 15; after 79 +/- 15 beats/min) and systolic aortic pressure (before 147 +/- 27; after 149 +/- 28 mmHg). Following intravenous administration, the mean coronary diameter decreased by 20% (1.90 +/- 0.6 mm; p less than 0.01 vs intracoronary dose) and the heart rate diminished slightly (76 +/- 12 beats/min; p less than 0.01). Nevertheless, the systolic aortic pressure did increase by 16% (171 +/- 28 mmHg; p less than 0.001). No major complications were observed and the appearance of side effects was minimal. Thus, the intracoronary delivery route, at the applied dosage, induces lesser vasoconstriction than usual intravenous administration, and systemic effects, such as hypertension, are avoided.     

Regional left ventricular mechanical function during isometric exercise in patients with coronary artery disease: correlation with regional coronary blood flow changes

The effects of isometric exercise on regional left ventricular mechanical function and regional coronary blood flow were evaluated in 17 patients with significant proximal stenosis of the left anterior descending coronary artery and 10 patients with normal coronary arteriograms. All patients had normal myocardial contractility in the basal condition. All performed isometric handgrip exercise at 50% of the maximal voluntary contraction for 3 min during two-dimensional echocardiographic monitoring and hemodynamic evaluation of great cardiac vein flow by thermodilution technique. During isometric exercise, 7 of the 17 patients with left anterior descending coronary stenosis developed asynergy in the anterior territory (anterior or septal segment, or both) (group I); the remaining 10 showed normal myocardial contraction during the test (group II). The 10 normal subjects manifested no regional asynergy during the test (control group). The increase in great cardiac vein flow at peak isometric exercise was significantly smaller (p less than 0.01) in group I (+15 +/- 8%) than that in group II (+98 +/- 48%) and the control group (+64 +/- 22%). Anterior coronary vascular resistance decreased in group II (-32 +/- 13%) and in the control group (-25 +/- 8%) but increased in group I (+6 +/- 8%, p less than 0.01 versus group II and control group). These data demonstrate that handgrip-induced myocardial asynergy is associated, in our study patients, with an abnormal response of the regional coronary circulation. The increase in coronary vascular resistance in group I patients with asynergy demonstrates that functional mechanisms play a dominant role in left ventricular mechanical dysfunction induced by isometric exercise.