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1.
Int J Cardiol ; 33(1): 75-81, 1991 Oct.
Article in English | MEDLINE | ID: mdl-1937985

ABSTRACT

UNLABELLED: In a single-blind, placebo-controlled, crossover trial versus diltiazem, we evaluated the influence of gallopamil on cardiovascular responses evoked by bicycle exercise. Twelve patients with chronic stable angina were enrolled. After a 5 days placebo run-in period, patients were randomly assigned either to gallopamil (50 mg thrice daily) or diltiazem (60 mg thrice daily) for 10 days. Then, patients were changed to the alternative drug. After placebo, and at the end of each subsequent period, all subjects underwent right heart catheterization by means of a Swan-Ganz thermodilution catheter. Hemodynamics were determined in 3 ways: supine, standing and during a multistage exercise test. RESULTS: anginal attacks were reduced to a similar degree by gallopamil (2.1 +/- 1/week versus 5.8 +/- 2.8/week during placebo, p less than 0.01) and diltiazem (2.0 +/- 0.8/week versus 5.8 +/- 2.8/week during placebo, P less than 0.01). At rest, gallopamil caused a significant decrease in heart rate and a slight fall in systemic vascular resistance. Cardiac index rose during exercise and was higher with respect to placebo at peak exercise (6.7 vs 5.6 l/min/m2, P less than 0.05). As a consequence, stroke volume index and stroke work index both increased at maximum workload (P less than 0.05). Compared to placebo, exercise time was significantly improved by gallopamil (+50%, P less than 0.02) and diltiazem (+38%, P less than 0.05). Likewise, time to onset of ST-segment depression was prolonged by 70% with gallopamil (P less than 0.01) and by 64% with diltiazem (P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Coronary Disease/drug therapy , Gallopamil/therapeutic use , Adult , Cardiac Catheterization , Coronary Disease/diagnosis , Diltiazem/therapeutic use , Electrocardiography , Exercise/physiology , Exercise Test , Humans , Male , Middle Aged , Myocardium/metabolism , Single-Blind Method
3.
Minerva Cardioangiol ; 37(5): 259-64, 1989 May.
Article in Italian | MEDLINE | ID: mdl-2779805

ABSTRACT

UNLABELLED: In an open non-comparative clinical study, 19 patients with spontaneous angina pectoris admitted to hospital with attacks lasting greater than 10 minutes, unresponsive to nitrate and/or calcium antagonist treatment, at least 2 ECG readings of raised (greater than or equal to 1.5 mm) or lowered (greater than or equal to 1 mm) ST segment not attributable to earlier AMI in the same area, were treated after the interruption of conventional treatment (mean 47 +/- 34.2 min) with 2 million IU endovenous UK in 15 mins followed by 1 million IU endovenous UK in 60 mins. Sixty minutes after UK administration was terminated, they were given a bolus of 5000 IU calcium heparin, followed by 1000 IU per hour for 2 days. Coronary angiography (Judkins technique) was performed before the start of UK treatment and 15, 30, 45, 60 and 75 minutes into it. RESULTS: Basal coronarography showed only "multiple organic stenosis" in 5 out of the 19 patients, a more complex situation suggestive of thrombi in the coronary arteries in 14. Subsequent angiographies (mean 30 mins later) revealed coronarographic improvement in 11 out of the 19 (58%), or 11 out of 14 (78.5%) if we exclude those with simple stenosis. Angina attacks were significantly lower in the 8 days after UK treatment than in the week before it in terms of number (4 v. 1; p less than 0.01), global severity (7 v. 1.5; p less than 0.01) and global duration (45 v. 4.25 min; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Angina Pectoris/drug therapy , Urokinase-Type Plasminogen Activator/therapeutic use , Angina Pectoris/diagnostic imaging , Coronary Angiography , Female , Humans , Injections, Intravenous , Male , Middle Aged , Urokinase-Type Plasminogen Activator/administration & dosage
4.
Jpn Heart J ; 29(2): 179-87, 1988 Mar.
Article in English | MEDLINE | ID: mdl-3398251

ABSTRACT

To determine whether post-reperfusion acute Q waves are due to irreversible myocardial necrosis, we studied the relationship between abnormal Q waves and left ventricular regional wall motion in 74 patients who had coronary thrombolysis following acute myocardial infarction. In 48 cases, acute pathologic Q waves appeared on the ECG-recordings after coronary reperfusion (group A), whereas in 26 patients the QRS complex had no or only minimal changes (group B). A control group consisted of 27 patients with unsuccessful thrombolysis. Quantitative left ventricular angiography was performed after coronary thrombolysis and repeated before discharge from the hospital. Regional wall motion of the infarcted area was determined by a system of 48 radii traced from the centroid of the end-diastolic and end-systolic silhouettes. Myocardial akinesis was significantly more extensive in group A than in group B (18 +/- 9% vs. 10 +/- 6%, p less than 0.02). Regional wall motion of the infarcted area improved in both groups at predischarge study (mean radial shortening +5 +/- 6% in group A and +4 +/- 7% in group B). Moreover, regional wall motion was significantly better in group A with respect to the control group (angio score of hypo-akinesis 166 +/- 124 vs. 412 +/- 174, p less than 0.01). In conclusion, post-reperfusion abnormal Q waves 1) are associated with more extensive myocardial damage, 2) do not preclude late recovery of ischemic myocardium, and 3) do not necessarily indicate irreversible transmural necrosis.


Subject(s)
Angiocardiography , Electrocardiography , Myocardial Contraction , Myocardial Infarction/physiopathology , Heart Ventricles/diagnostic imaging , Humans , Myocardial Infarction/diagnostic imaging , Myocardial Infarction/pathology , Myocardium/pathology
5.
G Ital Cardiol ; 17(5): 391-6, 1987 May.
Article in Italian | MEDLINE | ID: mdl-3653596

ABSTRACT

UNLABELLED: Clinical outcome after coronary thrombolysis are strictly related to the residual stenosis. However, the natural history of this lesion is largely unknown. To assess this topic we evaluated 25 patients who had coronary recanalization by urokinase in acute myocardial infarction. Serial coronary angiograms were taken immediately after fibrinolytic therapy, before hospital discharge and 1 year later. Angiographically detected coronary reocclusion and/or new ischemic events were exclusion criteria. Angiographic analysis was performed at a five-fold magnification. The followings were specifically evaluated: a) vessel contours at the site of the residual stenosis; b) luminal diameter reduction; c) presence of intraluminal filling defects. RESULTS: the vessel narrowing progressively improved from the acute phase (percent of stenosis 92 +/- 7) to the hospital discharge (82 +/- 8%, p less than .01) and to 1 year follow-up (76 +/- 11%, p less than .001 vs hospital discharge). Moreover, the residual stenosis appears to be "complicated" in early period (irregular contours with superimposed thrombus), but become regular and "uncomplicated" at follow-up examination (smooth contours, hourglass configuration, no intraluminal filling defects). IN CONCLUSION: a) the residual coronary stenosis is a dynamic process and may improve at follow-up examination; b) a practical approach to the management of the residual stenosis must take in account the natural history of the lesion to give a correct indication for coronary surgery or PTCA.


Subject(s)
Coronary Artery Disease/physiopathology , Fibrinolysis , Adult , Aged , Coronary Artery Disease/drug therapy , Coronary Artery Disease/pathology , Female , Follow-Up Studies , Humans , Male , Middle Aged , Remission Induction , Urokinase-Type Plasminogen Activator/therapeutic use
6.
G Ital Cardiol ; 17(5): 450-5, 1987 May.
Article in Italian | MEDLINE | ID: mdl-3653603

ABSTRACT

Since Ca++-overloading is a major problem after myocardial reperfusion we studied the effects of Diltiazem on the left ventricular diastolic function in the early days following coronary thrombolysis. Twelve patients who had myocardial reperfusion by intracoronary urokinase in acute myocardial infarction were admitted to the study. Previous infarct, cardiogenic shock or late thrombolysis (greater than 4 h from symptoms onset) were exclusion criteria. All subjects were evaluated at control cardiac catheterization 5-8 days after the acute ischemia. Simultaneous left ventricular angiography and high-fidelity pressure recordings by means of a tip-micromanometer and angiographic catheter were performed at rest and after intravenous Diltiazem administration (16 mg over 2' + 0.008 mg/Kg/min). Indexes of myocardial relaxation and early ventricular filling were impaired at rest but improved significantly after Diltiazem (Tab. II). Isovolumic relaxation period fell from 92 +/- 8 msec to 77 +/- 12 msec (p less than .01), T constant of isovolumic pressure decay decreased from 61 +/- 7 msec to 55 +/- 7 msec (p = ns), first-third of filling rate increased from 64 +/- 7% to 79 +/- 6% (p less than .01). On the other hand, indexes of left ventricular compliance were altered after coronary reperfusion (left ventricular end-diastolic compliance 17 +/- 13 mmHg-1. 10(-3), modulus of chamber stiffness .045 +/- .008) but but did not change after calcium-blocker therapy. In conclusion, post-thrombolysis diastolic function is severely impaired at rest, probably because of raised intracellular Ca++ and delayed asynchronous relaxation. Diltiazem improves energy-dependent early diastole, but does not affect ventricular compliance.


Subject(s)
Coronary Circulation , Diastole/drug effects , Diltiazem/pharmacology , Fibrinolysis , Myocardial Contraction/drug effects , Myocardial Infarction/drug therapy , Adult , Aged , Humans , Male , Middle Aged , Myocardial Infarction/physiopathology , Systole/drug effects
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