Biomedical subjects

A Castaigne

Publications and source records attributed to A Castaigne.

At least 37 records · Page 2Linked to original sources

PubMed1999

Prognostic value of MIBG imaging in idiopathic dilated cardiomyopathy.

UNLABELLED: Alterations of cardiac sympathetic innervation are likely to contribute to fatal outcomes in patients with heart failure. These alterations can be evaluated noninvasively by 123I-metaiodoben-zylguanidine (MIBG) imaging. METHODS: The hypothesis that impaired cardiac sympathetic innervation, as assessed using MIBG imaging, is related to adverse outcomes was tested in 112 patients with heart failure resulting from idiopathic cardiomyopathy. Main inclusion criteria were New York Heart Association classes II-IV and radionuclide left ventricular ejection fraction (LVEF) < 40%. Patients were assessed for cardiac MIBG uptake, circulating norepinephrine concentration, LVEF, peak Vo2, x-ray cardiothoracic ratio, M-mode echographic end-diastolic diameter and right-sided heart catheterization parameters. RESULTS: During a mean follow-up of 27 +/- 20 mo, 19 patients had transplants, 25 died of cardiac death (8 sudden deaths), 2 died of noncardiac death and 66 survived without transplantation. The only independent predictors for mortality were low MIBG uptake (P < 0.001) and LVEF (P = 0.02) when using multivariate discriminant analysis. Moreover, MIBG uptake (P < 0.001) and circulating norepinephrine concentration (P = 0.001) were the only independent predictors for life duration when using multivariate life table analysis. CONCLUSION: Impaired cardiac adrenergic innervation as assessed by MIBG imaging is strongly related to mortality. MIBG imaging may help risk stratify patients with heart failure resulting from idiopathic dilated cardiomyopathy.

3-Iodobenzylguanidine↗

PubMed1999

[Hypertrophic obstructive cardiomyopathy and double-chamber pacing. Long-term results in a consecutive series of 22 patients].

The authors report their experience with dual-chamber pacing in hypertrophy obstructive cardiomyopathy. 22 patients (14 women and 8 men) mean age 60 +/- 13 years were implanted between 1992 and 1998. The criteria for pace-maker implantation were the presence of severe symptoms related with hypertrophy obstructive cardiomyopathy (dyspnea, angina, syncope) and left ventricular outflow tract gradient at mean 30 mmHg. Before pacing, all patients received a medical therapy which included beta-blockers or calcium inhibitors. This treatment was considered as ineffective or responsible of side effects. Patients were followed-up at mean 35.1 +/- 20.3 months. During this period, symptoms improved (mean NYHA class 2.7 +/- 0.5 before pacing vs 1.4 +/- 0.5 after pacing) and left ventricular outflow tract lowered from 95.4 +/- 40.8 to 39.3 +/- 20.5 at 6 months. 34.3 +/- 23.4 at one year and 26.5 +/- 21 at the end of follow-up. Seven patients had RF ablation of atrio-ventricular junction for paroxysmal atrial fibrillation or for lack of hemodynamic improvement with pacing. This procedure permits a significative lowering of gradient and a better ventricular filling. In conclusion, dual-chamber pacing is effective for treatment of hypertrophy obstructive cardiomyopathy when medical therapy is ineffective or bad tolerated at condition of: perfect pacing with permanent ventricular capture and optimal AV delay; RF ablation of AV junction in one third of cases; medical therapy systematically associated in all patients.

Cardiac Pacing, Artificial↗

PubMed1998

Comparison of regional myocardial velocities assessed by quantitative 2-dimensional and M-mode color Doppler tissue imaging: influence of the signal-to-noise ratio of color Doppler myocardial images on velocity estimators of the Doppler tissue imaging system.

M-mode color Doppler imaging of the myocardium affords a greater sampling rate and signal-to-noise (S/N) ratio than 2-dimensional (2D) imaging. In this study, we compared myocardial velocities assessed by 2D and M-mode Doppler tissue imaging (DTI) at the same site and evaluated the influence of the S/N ratio on velocity estimates of the currently used DTI systems. In patients with and without impaired regional left ventricular function, myocardial velocities assessed by 2D DTI were lower than those obtained with M-mode DTI. The difference between regional velocities derived from both imaging techniques was positively correlated with the extent of the "black zone," which could be considered as indirectly reflecting the S/N ratio for each frame. Thus in the clinical setting and on currently used echocardiographs, 2D DTI may provide underestimated regional myocardial velocities when compared with M-mode, mainly because of the influence of the lower sampling rate and S/N ratio on velocity estimators of the imaging system.

Echocardiography, Doppler, Color↗

PubMed1998

Relation between impairment in nitric oxide pathway and clinical status in patients with congestive heart failure.

A dissociation between basal and stimulated release of nitric oxide (NO) has been found in the peripheral vasculature of patients with congestive heart failure. To explore basal and stimulated NO-mediated vasodilation in patients with heart failure of varying severity, three groups of subjects were studied: group 1, eight normal subjects; group 2, six patients with moderate heart failure; and group 3, eight patients with severe heart failure. Forearm blood flow (FBF) was measured by plethysmography in response to local brachial infusion of acetylcholine, N(G)-monomethyl-L-arginine (L-NMMA), sodium nitroprusside (SNP), and noradrenaline (NA). The vasodilating response to acetylcholine was markedly impaired in patients with severe heart failure compared with the other groups, with FBF increasing by 59 +/- 19% in group 3 vs. 220 +/- 64% in group 2 (p < 0.05) and 586 +/- 168% in group 1 (p < 0.01) at 80 microg/min acetylcholine. As compared with controls, vasodilation to SNP was impaired in group 3 but unchanged in group 2. NA caused similar vasoconstrictor response in the three groups, whereas vasoconstriction to L-NMMA was less marked in group 3. These results show that vasodilator responses to both acetylcholine and SNP are impaired in patients with heart failure and that this impairment is related to the clinical severity of heart failure.

Acetylcholine↗

PubMed1998

[Effects of high sodium intake on ventricular remodeling in mice].

BACKGROUND: Despite extensive research, controversy still exists regarding the role of dietary sodium intake on hypertension and left ventricular (LV) hypertrophy. Echocardiography is a powerful tool to assess LV hypertrophy and recent technical developments allow now its use in small animals. METHODS: We examined the effect of high sodium intake on LV geometry using echocardiography in mice. Three groups of Swiss mice were submitted, for 8 weeks, to different salt diets (0.6, 2 and 4% NaCl; n = 12, n = 8 and n = 12 respectively). LV end-diastolic (ED) septal and posterior wall thicknesses, LV ED diameter were measured at baseline, 4 and 8 weeks. RESULTS: At baseline, heart rate, LV ED septal and posterior wall thicknesses and LV ED diameter were similar between groups. At 8 weeks, for similar heart rate, LV ED posterior wall thickness were not different (0.6%: 0.64 +/- 0.01, 2%: 0.62 +/- 0.08 and 4%: 0.67 +/- 0.03 mm respectively) but LV septal wall thickness ass increased in a salt diet dependent manner (0.6%: 0.63 +/- 0.01, 2%: 0.75 +/- 0.01, 4%: 0.80 +/- 0.02 mm, p < 0.01). This increase was correlated with urinary sodium excretion (r = 0.84, p < 0.01) but occurred in the absence of change in arterial pressure (tail-cuff plethysmography; 0.6%: 135 +/- 6.2%: 127 +/- 4 and 4%: 139 +/- 9 mmHg respectively). The in-vivo interventricular septal remodeling was confirmed in perfused fixed preparations of hearts. CONCLUSION: Echocardiography allows precise measurements of regional LV wall dimensions in mice, and high sodium intake, in the absence of hypertension, induces interventricular septal remodeling.

Animals↗

PubMed1998

[Heart and brain: are the risk factors the same? Are the results of primary and secondary trials comparable?].

The aim of this study was to identify the similitudes and the differences in the epidemiology and prevention of myocardial infarction and cerebrovascular accidents by analysis of trials of primary and secondary prevention of myocardial infarction and cerebrovascular accidents. The principal risk factors common to both pathologies are hypertension, smoking and increased LDL-cholesterol. However, the statistical significance with respect to causality differs from one pathology to the other. Similarly, the impact of preventive measures is not the same: the treatment of hypertension is more important in the prevention of cerebrovascular accidents than myocardial infarction; the situation is the other way around with respect to the treatment of hypercholesterolaemia. Of the therapeutic interventions, aspirin is effective in all stages of coronary artery disease but does not prevent cerebrovascular accidents in patients without documented atherosclerosis. Thrombolysis carries a much higher benefit/risk ratio in the treatment of myocardial infarction than in that of cerebral infarction. The so-called cardioprotective drugs, such as the betablockers and angiotensin converting enzyme inhibitors, have only been used to any extent in the secondary prevention of myocardial infarction. These differences reflect the fact that cerebrovascular accident covers a range of diseases much more diverse than does myocardial infarction, and also that the brain is much more exposed to haemorrhage whereas cardiac haematoma is highly unusual. Finally, cerebral atherosclerosis is a later event than coronary atherosclerosis and this has epidemiological implications which are difficult to assess. In conclusion, the prevention of myocardial infarction and of cerebrovascular accidents may proceed theoretically by a common pathway but in practice, it is very different.

Arteriosclerosis↗

PubMed1998

[Physiopathological basis of the treatment of heart failure].

Therapeutic advances have changed the mode of presentation of cardiac failure over the last decades: the main cause, nowadays, is myocardial ischaemia. The modern treatment of cardiac failure is based on relatively simple physiopathological mechanisms which take into account the different aspects of cardiac physiology: a pump, a muscle, a coronary circulation supplying oxygen to the myocardium, an automatic contraction. The concept of vasodilatation and the blocking of vasoconstrictive systems introduced during the 70s is the basis of modern treatment of cardiac failure which involves angiotensin converting enzyme inhibitors and, increasingly, betablockers. In the near future, with earlier treatment of cardiac failure, the stimulation of vasodilator systems could become a new therapeutic strategy. Early detection of ischaemia and its complications with the aim of limiting the loss of cardiac myocytes is a priority for slowing the progression of cardiac failure. The prevention of cardiac failure also depends on educating cardiologists to treat rapidly the factors predisposing to or prolonging episodes of even mild cardiac failure.

Cardiology↗

PubMed1998

Study population and treatment titration in the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT).

OBJECTIVES: To ascertain the baseline characteristics of the high-risk hypertensive patients entering the International Nifedipine GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT). To determine the success of single and combination therapy in achieving target blood pressures in such a population. DESIGN: INSIGHT is a double-blind, prospective outcome trial comparing the efficacy of the calcium channel blocker, nifedipine GITS, and the thiazide, co-amilozide, in preventing myocardial infarction and stroke. We recruited 2996 men and 3454 women, aged 55-80 years, with blood pressure during placebo run-in >150/95 mmHg or isolated systolic blood pressure >160 mmHg from nine countries. Treatment allocation to nifedipine GITS 30 mg daily or co-amilozide (hydrochlorothiazide 25 mg/amiloride 5 mg) once daily was performed by minimization rather than randomization to balance additional risk factors. This was followed by four optional increases in treatment: dose-doubling of the primary drug, addition of atenolol 25/50 mg or enalapril 5/10 mg, and then any other hypotensive drug excluding calcium blockers or diuretics. Target blood pressure was 140/90 mmHg or a fall > or = 20/10 mmHg. RESULTS: Blood pressure at randomization was 172+/-15 / 99+/-9 mmHg. Thirteen per cent of the patients were previously untreated. The proportions of each additional risk factors were: smoking > 10/day, 29%; cholesterol > 6.43 mmol/l, 52%; family history of premature myocardial infarction or stroke, 21%; diabetes mellitus 20%; left ventricular hypertrophy, 10%; previous myocardial infarction, other presentations of coronary heart disease, and peripheral vascular disease, each 6%; proteinuria, 3%. Fifty-five per cent of patients had one additional risk factor, whereas 33%, 9% and 3% had two, three or more additional risk factors, respectively. The blood pressure (and falls in blood pressure) at the end of titration and at 1 year after minimization was 139+/-12 / 82+/-7 mmHg (33+/-15 / 17+/-9) in the 5226 patients still on randomized treatment The numbers requiring the four treatment increments were, respectively, 1591, 780, 597 and 294, meaning that almost 70% of patients on randomized treatment in INSIGHT are receiving only the primary drug. At one year, 69% of patients had a blood pressure < or = 140/90 mmHg. CONCLUSION: INSIGHT is one of the first double-blind comparisons of active antihypertensive treatments, requiring high-risk patients to achieve sufficient power. Despite this requirement, it is possible to achieve good blood pressure control in most patients without the addition of multiple additional treatments that may dilute any differences between the primary agents.

Aged↗

PubMed1997

Is left atrial appendage flow a predictor for outcome of cardioversion of nonvalvular atrial fibrillation? A transthroacic and transesophageal echocardiographic study.

Accurate echocardiographic parameters for predicting the success of cardioversion or maintenance of sinus rhythm are poorly defined. This prospective transthoracic and transesophageal echocardiographic study was conducted to test the hypothesis that the left atrial appendage flow pattern could be a predictive parameter of the success of cardioversion and maintenance of sinus rhythm in patients with nonvalvular atrial fibrillation. Eighty-two consecutive patients with nonvalvular atrial fibrillation of <6 months' duration underwent transesophageal examination after transthoracic echocardiography. After exclusion of left atrial thrombus, pharmacologic (n = 18) or electrical (n = 64) cardioversion was successful in 75 of 82 patients. In the group that underwent successful cardioversion, maintenance of sinus rhythm (n = 35) or recurrence of arrhythmia (n = 40) was assessed during a 1-year follow-up. During transesophageal examination, five left atrial appendage thrombi were found, spontaneous echo contrast was present in 26 (32%) patients, and mean peak left atrial appendage emptying velocity was 35 +/- 18 cm/sec. Peak left atrial appendage emptying velocity was found to be statistically related to parameters of left ventricular and left atrial function but not to long-term maintenance of sinus rhythm. No other echocardiographic parameter was identified as a predictor for either the success of cardioversion or the maintenance of sinus rhythm at follow-up. In patients with nonvalvular atrial fibrillation of recent onset, peak left atrial appendage emptying velocity appears to be a complex parameter depending on left atrial and left ventricular function but that does not predict either the success rate of cardioversion or long-term maintenance of sinus rhythm after successful cardioversion.

Aged↗

PubMed1997

Alteration of left ventricular diastolic function during coronary angioplasty-induced ischemia: a color M-mode Doppler study.

OBJECTIVES: The aim of this study was to assess the effects of ischemia on diastolic function by analyzing flow propagation velocity with color M-mode Doppler echocardigraphy. BACKGROUND: Color M-mode Doppler echocardiography has been proposed as a method of assessing left ventricular filling. METHODS: Color M-mode Doppler echocardiography and measurement of hemodynamic data were performed simultaneously at baseline and during angioplasty-induced ischemia. Tau was compared with flow propagation velocity. Late diastolic indexes, left ventricular pressure and flow cessation time were also investigated. RESULTS: During ischemia, left ventricular relaxation rate (tau) increased, whereas flow propagation velocity decreased, from (mean +/- SD) 46.8 +/- 10 ms to 72.6 +/- 18.3 ms and from 59.8 +/- 15.8 cm/s to 30 +/- 8 cm/s, respectively (all p < 0.0001). The maximal slowing of flow propagation velocity was observed 20 to 30 s after the beginning of the inflation, coexisting with a notch on the ascending limb of the negative rate of rise of the left ventricular pressure (dP/dt) curve. Flow propagation velocity was correlated with tau both at baseline (r = 0.53, p < 0.05) and during inflation (r = 0.53, p < 0.03). Left ventricular end-diastolic pressure increased during ischemia from 13.5 +/- 8 mm Hg at baseline to 27.5 +/- 7 mm Hg, while a premature cessation of the entering flow occurred -13.8 +/- 23 ms before the next Q wave onset, compared with 4.5 +/- 19.6 ms after the Q wave onset at baseline (all p < 0.0001). CONCLUSIONS: The analysis of flow propagation velocity showed that early filling is highly dependent on left ventricular relaxation rate, particularly through the phenomenon of asynchrony. During ischemia, the premature cessation of late filling is associated with increased diastolic pressures.

Angioplasty, Balloon, Coronary↗

PubMed1997

Effect of pravastatin on angiographic restenosis after coronary balloon angioplasty. The PREDICT Trial Investigators. Prevention of Restenosis by Elisor after Transluminal Coronary Angioplasty.

OBJECTIVES: This study sought to determine whether pravastatin affects clinical or angiographic restenosis after coronary balloon angioplasty. BACKGROUND: Experimental data and preliminary clinical studies suggest that lipid-lowering drugs might have a beneficial effect on restenosis after coronary angioplasty. METHODS: In a multicenter, randomized, double-blind trial, 695 patients were randomized to receive pravastatin (40 mg/day) or placebo for 6 months after successful balloon angioplasty. All patients received aspirin (100 mg/day). The primary angiographic end point was minimal lumen diameter (MLD) at follow-up, assessed by quantitative coronary angiography. A sample size of 313 patients per group was required to demonstrate a difference of 0.13 mm in MLD between groups (allowing for a two-tailed alpha error of 0.05 and a beta error of 0.20). To allow for incomplete angiographic follow-up (estimated lost to follow-up rate of 10%), 690 randomized patients were required. Secondary end points were angiographic restenosis rate (restenosis assessed as a categoric variable, > 50% stenosis) and clinical events (death, myocardial infarction, target vessel revascularization). RESULTS: At baseline, clinical, demographic, angiographic and lipid variables did not differ significantly between groups. In patients treated with pravastatin, there was a significant reduction in total and low density lipoprotein cholesterol and triglyceride levels and a significant increase in high density lipoprotein cholesterol levels. At follow-up the MLD (mean +/- SD) was 1.47 +/- 0.62 mm in the placebo group and 1.54 +/- 0.66 mm in the pravastatin group (p = 0.21). Similarly, late loss and net gain did not differ significantly between groups. The restenosis rate (recurrence > 50% stenosis) was 43.8% in the placebo group and 39.2% in the pravastatin group (p = 0.26). Clinical restenosis did not differ significantly between groups. CONCLUSIONS: Although pravastatin has documented efficacy in reducing clinical events and angiographic disease progression in patients with coronary atherosclerosis, this study shows that it has no effect on angiographic outcome at the target site 6 months after coronary angioplasty.

Adult↗

PubMed1997

[Echocardiographic factors predicting the maintenance of sinus rhythm one year after cardioversion for non-valvular atrial arrhythmias].

Echocardiographic factors predictive of the maintenance of sinus rhythm after successful cardioversion were investigated in 94 patients with non-valvular atrial arrhythmias of recent onset. Seventy-five patients with atrial fibrillation and 19 with atrial flutter admitted for reduction of their arrhythmias underwent transthoracic and transoesophageal echocardiography. After excluding a thrombus in the left atrial appendage or checking that it had disappeared (5 patients), and electrical (n = 74) or pharmacological (n = 20) cardioversion was successfully performed. The maintenance of sinus rhythm (n = 44) or recurrence of arrhythmia (n = 50) were controlled every 3 months for one year. The mean value of the peak positive blood flow in the left atrial appendage was 38 +/- 20 cm/s for the whole group. It was not possible to identify an echocardiographic parameter predictive of maintenance of sinus rhythm at one year either in the whole group or in the subgroups with atrial flutter or atrial fibrillation. In the group in atrial flutter, the mean value of the peak positive blood flow in the left atrial appendage was significantly greater than in the group with atrial fibrillation: 49 +/- 22 cm/s vs 35 +/- 18 cm/s, respectively; p < 0.05. The peak of positive flow in the left atrial appendage was statistically related to indirect parameters of left atrial function and of left ventricular function in the group with atrial fibrillation but only with parameters of left ventricular function in the smaller group with atrial flutter.

Aged↗

PubMed1996

Endogenous sodium-potassium-chloride cotransport inhibitor in congestive heart failure.

OBJECTIVES: This study sought to evaluate the relation, if any, between fluid overload in congestive heart failure (CHF) and a newly discovered endogenous natriuretic factor acting like loop diuretic drugs: cotransport inhibitory factor (CIF). BACKGROUND: The humoral mechanisms regulating volume overload in CHF are not fully understood. Therefore, we investigated whether there is a role for CIF in this pathologic condition. METHODS: Plasma and urinary CIF levels were investigated in 23 patients with chronic CHF and compared with changes in plasma atrial natriuretic peptide (ANP). Twelve patients without CHF served as control subjects. RESULTS: CHF was associated with a highly significant threefold increase in both plasma CIF levels (mean +/- SD 7.10 +/- 3.01 vs. 2.28 +/- 0.92 U/ml, p < 0.0001) and urinary CIF excretion (7,849 +/- 3,600 vs. 2,351 +/- 1,297 U/day, p < 0.0001) with respect to patients without CHF. CIF increased as a function of impairment in left ventricular ejection fraction (r = -0.703, p < 0.0001) and the severity of clinical status. Plasma ANP was also increased in patients with CHF, although to a lesser extent (68%, p = 0.0501) than plasma CIF, and was also significantly correlated with left ventricular ejection fraction (r = -0.552, p = 0.0004). CONCLUSIONS: Plasma and urinary CIF activities were strongly and very significantly increased in chronic CHF. In addition to ANP, this long-term natriuretic agent may be of potential importance in reducing fluid overload in CHF.

Adult↗

PubMed1996

Sympathetic stimulation overrides flow-mediated endothelium-dependent epicardial coronary vasodilation in transplant patients.

BACKGROUND: Abnormal coronary vasomotor responses have been described in transplant patients. The aim of this study was to evaluate the graft epicardial vasomotor responses to different stimuli that increase coronary blood flow. METHODS AND RESULTS: Twelve heart transplant recipients with angiographically normal epicardial coronary arteries were compared 2.7 +/- 1.2 months after surgery with 6 control subjects. Coronary flow velocity was measured with a guidewire Doppler. Coronary diameter changes of the proximal and midportion of the left anterior descending coronary artery were assessed by quantitative coronary angiography during rapid atrial pacing, cold pressor test, supine exercise, and subselective infusion of papaverine and after intracoronary injection of linsidomine (SIN-1). Catecholamine plasmatic levels were determined at the different stages of the protocol. In 6 other transplant patients, a cold pressor test was performed before and after intracoronary infusion of phentolamine (10 micrograms.kg-1.min-1). Coronary flow velocity increased significantly in both groups during each phase of the protocol. In control subjects, dilation was observed in response to atrial pacing (8.7 +/- 7.6%; P < .05), CPT (8.8 +/- 2.3%; P < .01), exercise (14.5 +/- 9.4%; P < .001), and papaverine infusion (14.2 +/- 6.1%; P < .001) and after injection of SIN-1 (26.8 +/- 11.9%; P < .001). In transplant patients, similar dilation was observed during atrial pacing (8.2 +/- 8.3%; P < .05) and papaverine infusion (14.6 +/- 7.8%; P < .001) and after SIN-1 (25.8 +/- 10.8%; P < .001). CPT and exercise caused slight constriction (-3.5 +/- 4.5% and -2.7 +/- 10.5%, respectively; both P < .001 versus control subjects). Norepinephrine plasmatic levels increased in both groups during CPT and exercise. Slight constriction during the cold pressor test (-4.5 +/- 9.6%) changed to dilation (6.8 +/- 7.0%) after alpha-blockade with phentolamine (P < .001). CONCLUSIONS: These results show that flow-mediated, endothelium-dependent vasodilation is preserved early after trans-plantation. Sympathetic stimulation, which overrides the endothelium-dependent mechanism, can be related to hypersensitivity to catecholamines due to denervation.

Adrenergic alpha-Antagonists↗

PubMed1996

Effect of delayed percutaneous transluminal coronary angioplasty of occluded coronary arteries after acute myocardial infarction.

Whether angioplasty of occluded vessels after myocardial infarction may have beneficial effects on left ventricular function remains unknown. Patients with a first myocardial infarction and thrombolytic therapy who had an occluded infarct-related vessel at delayed coronary angiography were referred systematically for an elective coronary angioplasty performed between 3 and 4 weeks after the myocardial infarction. All patients underwent stress-redistribution-reinjection thallium-201 single-photon emission computed tomography for myocardial viability assessment. Prior angioplasty, a quantitative evaluation of global and regional left ventricular function, was performed. The study group consisted of 38 patients (aged 57 +/- 10 years); 18 had anterior wall infarctions and 20 inferior wall infarctions, but before angioplasty 3 had a patent artery and were excluded. Angioplasty was successful in 30 patients. At follow-up 13 patients (43%) had an occluded coronary artery. In contrast with patients with an occluded coronary artery at follow-up, those with a patent coronary artery had no left ventricular enlargement and had an improvement in both left ventricular ejection fraction (from 48 +/- 9% to 52 +/- 9.8%, p = 0.002) and regional wall motion index (delta = +0.95 SD, p <0.01). In patients with a patent vessel at follow-up, there was a positive correlation between the number of myocardial viable segments and improvement of the infarct zone wall motion (r = 0.52; p = 0.035), and the number of necrotic segments at baseline was positively correlated to the 4-month changes in end-diastolic volume indexes (r = 0.6; p = 0.04). Thus, elective revascularization of occluded coronary arteries with viable myocardium after myocardial infarction improves left ventricular function and lessens remodeling if the artery remains patent during follow-up.

Aged↗

PubMed1996

Usefulness of redistribution images in viability detection after acute myocardial infarction.

We undertook this study to evaluate the importance of redistribution images in thallium 201 single-photon emission computed tomography (Tl-201 SPECT) assessment of myocardial viability after acute myocardial infarction. Stress-redistribution-reinjection Tl-201 SPECT was performed in 55 consecutive patients with recent (within 1 month) acute myocardial infarction. The myocardium was divided into 16 segments and activity assessed visually with a score from 0 to 3 on stress-redistribution and stress-reinjection images. A defect was considered moderate if the stress score was 2 and severe if the stress score was 0 or 1. All moderate defects were considered viable, regardless of score on redistribution or reinjection images. Severe defects were considered viable if they were reversible (improvement of 1 score) on redistribution or reinjection images. Stress-redistribution and stress-reinjection images were visually analyzed and compared in terms of viability classification. On visual analysis, 461 segments (52%) were abnormal. One hundred eleven stress defects were moderate; of these, 28 were reversible on reinjection images only and 15 on redistribution images only. However, all of these segments were viable, regardless of the analysis chosen. Of 350 severe stress defects, 48 were reversible on reinjection and irreversible on redistribution images, and 4 were reversible on redistribution and irreversible on reinjection images. Therefore, in viability assessment, 48 segments were misclassified with stress-redistribution analysis, whereas only 4 segments were misclassified using stress-reinjection analysis. Although the usefulness of Tl-201 reinjection imaging is confirmed, redistribution images seem to be of little interest in post-myocardial infarction viability assessment.

Aged↗

PubMed1996

Ventricular fibrillation following administration of thrombolytic treatment. The EMIP experience. European Myocardial Infarction Project.

Reperfusion-induced ventricular fibrillation has been demonstrated in animal models of myocardial ischaemia, but no evidence exists for this in humans. The European Myocardial Infarction Project compared the efficacy and safety of pre-hospital thrombolytic therapy with that of hospital therapy. The objective of this study was to investigate the occurrence of reperfusion-induced ventricular fibrillation in acute myocardial infarction patients following thrombolytic therapy. In a double-blind multicentre trial, eligible patients were randomized to receive anistreplase at home followed by placebo in the hospital (A/P group), or placebo followed by anistreplase (P/A group). The occurrence of ventricular fibrillation, and other adverse events were recorded on specific study forms and could be attributed to defined time intervals. The incidence of ventricular fibrillation in the A/P group was significantly higher following the pre-hospital injection than in the P/A group (2.5% vs 1.6%; P = 0.021); the situation was reversed following the hospital injection (3.6% vs 5.3%; P = 0.002). No relationship was found between this excess of ventricular fibrillation and the patients' condition, with the exception of the site of the infarct. These results suggest the existence of reperfusion-induced ventricular fibrillation in patients developing myocardial infarction who receive thrombolytic treatment.

Anistreplase↗

PubMed1996

INSIGHT: international nifedipine GITS study intervention as a goal in hypertension treatment.

The objective of the study is to compare fatal and nonfatal cardiovascular endpoints in hypertensive patients randomised to the calcium-channel blocker, nifedipine GITS or a thiazide diuretic, co-amilozide. A total of 6592 patients from nine countries (UK, France, Israel, Spain, Italy, The Netherlands, Sweden, Denmark and Norway) will be recruited, aged 55-80 and with a blood pressure (BP) > or = 150/95 or > or = 160 mm Hg (systolic). All patients will have at least one other major cardiovascular risk factor. Patients will be minimised by country and risk factors and randomised to double-blind treatment with either nifedipine GITS or diuretic. After a single dose titration, additional treatment will be atenolol or enalapril (where beta-blockade is contra-indicated). After achieving a target BP of 140/90 mm Hg patients will be followed for a total of 3 years. Primary endpoints are myocardial infarction, stroke, subarachnoid haemorrhage, heart failure and sudden cardiac death. The study has a power of 80% at 5% significance to detect a difference between 8% event rate over 3 years in diuretic-treated patients and 6% in those receiving nifedipine.

Aged↗