Site of myocardial infarction. A determinant of the cardiovascular changes induced in the cat by coronary occlusion.
The influence of site of acute myocardial infarction on heart rate, blood pressure, cardiac output, total peripheral resistance (TPR), cardiac rhythm, and mortality was determined in 58 anesthetized cats by occlusion of either the left anterior descending (LAD), left circumflex or right coronary artery. LAD occlusion resulted in immediate decrease in cardiac output, heart rate, and blood pressure, an increase in TPR, and cardiac rhythm changes including premature ventricular beats, ventricular tachycardia, and occasionally ventricular fibrillation. The decrease in cardiac output and increase in TPR persisted in the cats surviving a ventricular arrhythmia. In contrast, right coronary occlusion resulted in a considerably smaller decrease in cardiac output. TPR did not increase, atrioventricular condition disturbances were common, and sinus bradycardia and hypotension persisted in the cats recovering from an arrhythmia. Left circumflex ligation resulted in cardiovascular changes intermediate between those produced by occlusion of the LAD or the right coronary artery. Mortality was similar in each of the three groups. We studied the coronary artery anatomy in 12 cats. In 10, the blood supply to the sinus node was from the right coronary artery and in 2, from the left circumflex coronary artery. The atrioventricular node artery arose from the right in 9 cats, and from the left circumflex in 3. The right coronary artery was dominant in 9 cats and the left in 3. In conclusion, the site of experimental coronary occlusion in cats is a major determinant of the hemodynamic and cardiac rhythm changes occurring after acute myocardial infarction. The cardiovascular responses evoked by ligation are related in part to the anatomical distribution of the occluded artery. (+info)
Hierarchy of ventricular pacemakers.
To characterize the pattern of pacemaker dominance in the ventricular specialized conduction system (VSCS), escape ventricular pacemakers were localized and quantified in vivo and in virto, in normal hearts and in hearts 24 hours after myocardial infarction. Excape pacemaker foci were localized in vivo during vagally induced atrial arrest by means of electrograms recorded from the His bundle and proximal bundle branches and standard electrocardiographic limb leads. The VSCS was isolated using a modified Elizari preparation or preparations of each bundle branch. Peacemakers were located by extra- and intracellular recordings. Escape pacemaker foci in vivo were always in the proximal conduction system, usually the left bundle branch. The rate was 43+/-11 (mean+/-SD) beats/min. After beta-adrenergic blockade, the mean rate fell to 31+/-10 beats/min, but there were no shifts in pacemaker location. In the infarcted hearts, pacemakers were located in the peripheral left bundle branch. The mean rate was 146+/-20 beats/min. In isolated normal preparations, the dominant pacemakers usually were in the His bundle, firing at a mean rate of 43+/-10 beats/min. The rates of pacemakers diminished with distal progression. In infarcted hearts, the pacemakers invariably were in the infarct zone. The mean firing rates were not influenced by beta-adrenergic blockade. The results indicate that the dominant pacemakers are normally in the very proximal VSCS, but after myocardial infarction pacemaker dominance is shifted into the infarct. Distribution of pacemaker dominance is independent of sympathetic influence. (+info)
Anti-heart autoantibodies in ischaemic heart disease patients.
One hundred and ninety-nine ischaemic heart disease (IHD) patients were studied with regard to the prevalence of anti-heart autoantibodies (AHA). The incidence of AHA in IHD patients was 1%: one out of 102 patients who suffered acute myocardial infarction (AMI), one out of seventy-two patients who suffered from acute coronary insufficiency (ACI), and none out of twenty-five patients with other signs and symptoms of IHD, had AHA in their sera. An additional 2% of patients who suffered from AMI developed detectable antibody levels during a follow-up period of 15 days. In comparison,, 53% of patients (eight out of fifteen) who underwent heart surgery and who had no AHA prior to operation, developed these antibodies in their sera during 1-2 weeks following operation. (+info)
Is hospital care involved in inequalities in coronary heart disease mortality? Results from the French WHO-MONICA Project in men aged 30-64.
OBJECTIVES: The goal of the study was to assess whether possible disparities in coronary heart disease (CHD) management between occupational categories (OC) in men might be observed and contribute to the increasing inequalities in CHD morbidity and mortality reported in France. METHODS: The data from the three registers of the French MONICA Collaborative Centres (MCC-Lille, MCC-Strasbourg, and MCC-Toulouse) were analysed during two period: 1985-87 and 1989-91. Acute myocardial infarctions and coronary deaths concerning men, aged 30-64 years, were included. Non-professionally active and retired men were excluded. Results were adjusted for age and MCC, using a logistic regression analysis. RESULTS: 605 and 695 events were analysed for 1985-87 and 1989-91, respectively. Out of hospital cardiac arrests, with or without cardiac resuscitation, and 28 day case fatality rates were lower among upper executives in both periods. A coronarography before the acute event had been performed more frequently in men of this category and the proportion of events that could be hospitalised was higher among them. In both periods, the management of acute myocardial infarctions in hospital and prescriptions on discharge were similar among occupational categories. CONCLUSIONS: For patients who could be admitted to hospital, the management was found to be similar among OCs, as was the 28 day case fatality rate among the hospitalised patients. In contrast, lower prognosis and higher probability of being hospitalised after the event among some categories suggest that pre-hospital care and the patient's conditions before the event are the primary factors involved. (+info)
Optimal thrombolytic strategies for acute myocardial infarction--bolus administration.
Optimal strategies for thrombolysis in myocardial infarction (TIMI) are still being sought because the TIMI 3 flow rates achievable using standard regimens average approximately 60%. Double bolus administration of recombinant tissue plasminogen activator (tPA) is a novel approach with potential for earlier patency combined with ease of administration. We reviewed total patency rates, TIMI 3 patency rates, mortality, stroke and intracranial haemorrhage rates in the major trials of accelerated infusion tPA/bolus tPA/reteplase in acute myocardial infarction. A direct comparison was performed with results of two recent trials of double bolus (two 50 mg boli, 30 min apart) vs. accelerated infusion tPA: the Double Bolus Lytic Efficacy Trial (DBLE), an angiographic study, and the COBALT Trial, a mortality study. The DBLE trial showed equivalent patency rates for accelerated infusion and double bolus administration of tPA. Reviewing other angiographic trials, total patency and TIMI 3 patency rates achievable with double bolus tPA were comparable to those with accelerated infusion tPA or bolus reteplase administration. The COBALT study demonstrated a 30-day mortality of 7.53% in patients treated with accelerated infusion tPA compared with 7.98% for double bolus tPA treated patients. The small excess in mortality with double bolus treatment was confined to the elderly; in those < or = 75 years, mortality rates were 5.6% and 5.7%, for double bolus and accelerated infusion, respectively, and rates for death or non-fatal stroke were 6.35% and 6.3%, respectively. Comparison with other trials demonstrated mortality, stroke and intracranial haemorrhage rates with double bolus treatment similar to those associated with either accelerated infusion tPA or bolus reteplase treatment. Double bolus administration of tPA to patients with acute myocardial infarction is associated with total patency, TIMI 3 patency, mortality, stroke and intracranial haemorrhage rates similar to those associated with either accelerated infusion of tPA or bolus reteplase. (+info)
Premature morbidity from cardiovascular and cerebrovascular diseases in women with systemic lupus erythematosus.
OBJECTIVE: To determine rates of morbidity due to cardiovascular and cerebrovascular diseases among women with systemic lupus erythematosus (SLE). METHODS: I used the California Hospital Discharge Database, which contains information on all discharges from acute care hospitals in California, to identify women with SLE who had been hospitalized for treatment of either acute myocardial infarction (AMI), congestive heart failure (CHF), or cerebrovascular accident (CVA) from 1991 to 1994. I compared the proportions of hospitalizations for each cause among women with SLE with those in a group of women without SLE, for 3 age strata (18-44 years, 45-64 years, and > or =65 years). RESULTS: Compared with young women without SLE, young women with SLE were 2.27 times more likely to be hospitalized because of AMI (95% confidence interval [95% CI] 1.08-3.46), 3.80 times more likely to be hospitalized because of CHF (95% CI 2.41-5.19), and 2.05 times more likely to be hospitalized because of CVA (95% CI 1.17-2.93). Among middle-aged women with SLE, the frequencies of hospitalization for AMI and CVA did not differ from those of the comparison group, but the risk of hospitalization for CHF was higher (odds ratio [OR] 1.39, 95% CI 1.05-1.73). Among elderly women with SLE, the risk of hospitalization for AMI was significantly lower (OR 0.70, 95% CI 0.51-0.89), the risk of hospitalization for CHF was higher (OR 1.25, 95% CI 1.01-1.49), and the risk of hospitalization for CVA was not significantly different from those in the comparison group. CONCLUSION: Young women with SLE are at substantially increased risk of AMI, CHF, and CVA. The relative odds of these conditions decrease with age among women with SLE. (+info)
Expression of skeletal muscle sarcoplasmic reticulum calcium-ATPase is reduced in rats with postinfarction heart failure.
OBJECTIVE: To determine whether heart failure in rats is associated with altered expression of the skeletal muscle sarcoplasmic reticulum Ca2+-ATPase (SERCA). METHODS: SERCA protein and mRNA were examined in the soleus muscles of eight female rats with heart failure induced by coronary artery ligation, six weeks after the procedure (mean (SEM) left ventricular end diastolic pressure 20.4 (2.2) mm Hg) and in six sham operated controls by western and northern analyses, respectively. RESULTS: SERCA-2a isoform protein was reduced by 16% (112 000 (4000) v 134 000 (2000) arbitrary units, p < 0.001), and SERCA-2a messenger RNA was reduced by 59% (0.24 (0. 06) v 0.58 (0.02) arbitrary units, p < 0.001). Although rats with heart failure had smaller muscles (0.54 mg/g v 0.66 mg/g body weight), no difference in locomotor activity was observed. CONCLUSIONS: These results may explain the previously documented abnormalities in calcium handling in skeletal muscle from animals with the same model of congestive heart failure, and could be responsible for the accelerated muscle fatigue characteristic of patients with heart failure. (+info)
Recurring myocardial infarction in a 35 year old woman.
A 35 year old woman presented with acute myocardial infarction without any of the usual risk factors: she had never smoked; she had normal blood pressure; she did not have diabetes; plasma concentrations of total cholesterol and high and low density lipoprotein cholesterol, fibrinogen, homocysteine, and Lp(a) lipoprotein were normal. She was not taking oral contraceptives or any other medication. Coronary angiography showed occlusion of the left anterior descending coronary artery but no evidence of arteriosclerosis. Medical history disclosed a previous leg vein thrombosis with pulmonary embolism. Coagulation analysis revealed protein C deficiency. The recognition of protein C deficiency as a risk factor for myocardial infarction is important as anticoagulation prevents further thrombotic events, whereas inhibitors of platelet aggregation are ineffective. (+info)