Left ventricular rupture threshold during the healing phase after myocardial infarction in the dog

The mechanical resistance of the infarcted left ventricle to rupture, or rupture threshold, was measured by the balloon technique 1-42 days after left anterior descending coronary artery ligation in 70 dogs: 26 without infarction (18 sham, 8 with ligation) and 44 with infarction. Rupture threshold in noninfarcted hearts was higher than in infarcted hearts (1168 +/- 165 (SD) vs. 754 +/- 223 mmHg (1 mmHg = 133.32 Pa), p less than 0.001) and did not change over 6 weeks. In contrast, rupture threshold in infarcted hearts decreased (p less than or equal to 0.05) after 14 days, the average value for 21-42 days being less than that for 1-14 days: 577 +/- 140 vs. 867 +/- 191 mmHg, p less than 0.001. Passive left ventricular stiffness in infarcted hearts was higher than for noninfarcted hearts throughout the 6 weeks during early filling (11.1 +/- 3.9 vs. 7.1 +/- 1.4 mmHg/mL, p less than 0.001) but decreased (p less than or equal to 0.05) after 14 days during the prerupture phase (11.3 +/- 5.3 vs. 6.2 +/- 3.0 mmHg/mL, p less than 0.005). Between 7 and 42 days, the infarct zone showed marked increase in hydroxyproline (10.0 +/- 2.0 vs. 48.8 +/- 19.7 mg/g dry weight, p less than 0.001), shrinkage (infarct size, 25 +/- 9 vs. 9 +/- 5% of the left ventricle, p less than 0.005), and thinning (infarct to normal wall thickness ratio, 0.83 +/- 0.11 vs. 0.51 +/- 0.09, p less than 0.001) but little further stretching (expansion index or the ratio of lengths of infarcted and noninfarcted segments, 1.14 +/- 0.10 vs. 1.28 +/- 0.17, p less than 0.2). A mild decrease (p less than 0.05) in left atrial pressure and increase (p less than 0.05) in diastolic area and fractional change in area (two-dimensional echocardiography) were detected at 6 weeks. The late decrease in rupture threshold and prerupture stiffness of the infarcted left ventricle and thinning of the scar suggest a late decrease in mechanical strength and resistance of the infarcted left ventricle to distension.     

Cardiac sympathetic nerve activity and ventricular fibrillation during acute myocardial infarction in a conscious sheep model

The association between cardiac sympathetic nerve activity (CSNA) and ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been assessed in conscious animal models. During the first 60 min post-MI, mean blood pressure (MBP), heart rate (HR), and CSNA were recorded continuously in 20 conscious sheep. Resistant sheep (group A, n = 10) were compared with susceptible sheep (group B, n = 10) who developed fatal VF (n = 7) or sustained ventricular tachycardia (VT, n = 3). The mean time to VF/VT was 28.1 +/- 3.3 min. In group B, MBP, HR, and CSNA were averaged at each consecutive minute from baseline at 14 min before the onset of VF/VT and compared with time-matched values in group A. When compared with those of group A, indexes of CSNA burst size increased before the onset of VF/VT: burst area/minute (F(13,208) = 2.17, P = 0.01) and burst area/100 beats (F(13,208) = 1.86, P = 0.04). By contrast, burst frequency indexes were not significantly different: burst frequency (F(13,208) = 1.6, P = 0.09) and burst incidence (F(13,208) = 1.48, P = 0.13). In group A, CSNA burst area/min and burst area/100 beats did not change across this time period (F(13,117) = 0.97, P = 0.5, F(13,117) = 0.96, P = 0.7) but increased with time in group B (F(13,91) = 2.3, P = 0.01; and F(13,91) = 2.25, P = 0.01). Between-group comparisons demonstrated no differences in time of onset of ventricular ectopic beats: 18.5 (range 12-24) in group A versus 15.0 min (range 7-22) in group B (Mann-Whitney U-test, P = 0.09). Pre-MI baroreflex slopes were similar: R-R slopes were 11.8 +/- 2 and 15.6 +/- 1.1 ms/mmHg (t(18) = -1.6, P = 0.14). CSNA slopes were -1.8 +/- 0.3 and -2.3 +/- 0.2%/mmHg (t(18) = -1.4, P = 0.2). An early increase in CSNA burst size indexes (before 60 min post-MI), mediated by an excitatory sympathetic reflex, is important in the genesis of VF/VT.     

Effects of left ventricular unloading on reperfusion-related AIVR in acute myocardial infarction

Accelerated idioventricular rhythm (AIVR) often occurs in the setting of acute myocardial infarction, specifically after reperfusion. We studied the direct left ventricular (LV) dynamic effects of AIVR compared with sinus rhythm. Furthermore, we observed an interesting finding of LV unloading on the occurrence of AIVR.     

Cardiac arrhythmias during experimental induction and management of myocardial infarction in the dog.

The experimental production of a myocardial infarction (MI) in the dog was achieved adopting a new catheter technique. After induction of the MI, a variety of arrhythmias appeared and were classified according to the Lown-classification as more or less severe. The therapy was achieved with antiarrhythmics class 1-111 (Vaughn-Williams classification) for late premature ventricular beats or couplets. Sinus tachycardia was often terminated by occular or sinus carotis pressure or a new selective sinus blocking agent. Results showed Amiodarone to be the drug of choice in the treatment of severe arrhythmias (Lown IV and V) like triplets or salves of extrasystolies. Ventricular fibrillation always resulted in the death of the animal, because fibrillation was not convertible by direct current cardioversion, endovenous injection of Lidocaine or even internal cardiac massage. The registration of hemodynamic parameters (left ventricular end diastolic pressure, wedge pressure, pulmonary and aortic pressure) was shown to be important in controlling the therapy, as well as blood gas and electrolyte analysis.     

Increased release of beta thromboglobulin during acute myocardial infarction

Beta thromboglobulin (betaTG) is a platelet-specific protein released during platelet aggregation. To classify the role of platelet aggregation in acute myocardial infarction (AMI), betaTG levels were measured by means of a specific and highly sensitive radioimmunoassay in patients admitted to the Coronary Care Unit for the evaluation of acute chest pain. These levels were compared to creatine phosphokinase (CPK) values and the percentage of myocardial fraction (MB), as well as electrocardiographic criteria for AMI. Beta thromboglobulin was considered elevated when it was greater than 132 micro/1. The CPK and MB fraction were considered to indicate AMI if there was an increase of MB fraction greater than 5% of the total CPK and a progressive increase of the total CPK and MB fraction during the course of the disease. Ten patients were compared to 28 control subjects. Seven patients had electrocardiographic evidence of AMI in addition to CPK and MB criteria. Six of these patients also had elevated betaTG values, whereas one did not. This patient was admitted late during his clinical course, as evidenced by the CPK-MB curve. Of the three patients without clinical evidence of AMI, two had normal betaTG levels, whereas the third patient had one normal betaTG level and one mildly elevated level. This study implicates the role of platelet aggregation in AMI and suggests its potential usefulness as a diagnostic aid in evaluating acute chest pain.     

Improved myocardial performance induced by clofibrate during reperfusion after acute myocardial infarction

The increase of cellular fatty acids appears to be one of the causes of the myocardial injury during ischemia and reperfusion. This study was designed to examine whether a hypolipidemic drug such as clofibrate can reduce the myocardial injury during ischemia and reperfusion. Clofibrate was fed to experimental pigs for 9 days. Isolated in situ hearts from both experimental and control pigs were subjected to 60 min of regional ischemia induced by occluding the left anterior descending coronary artery, followed by 60 min of global ischemia by hypothermic cardioplegic arrest and 60 min of reperfusion. The clofibrate feeding resulted in the better cardiac performance as judged by increased coronary blood flow, improved left ventricular function, and reduced myocardial injury as judged by creatine kinase release. Although the clofibrate-fed animals contained higher levels of thiobarbituric reactive materials, the free fatty acid levels of plasma and myocardium were much lower compared with control animals. The clofibrate feeding was also associated with increased peroxisomal catalase and beta-oxidation of fatty acids. These results suggest that decreased levels of free fatty acids in the plasma and the myocardium and increased catalase activity induced by antilipolytic therapy appear to provide beneficial effects to the myocardium during ischemia and reperfusion.     

Right ventricular dysfunction following acute myocardial infarction in the absence of pulmonary hypertension in the mouse

Background

Cardiac remodelling after AMI is characterized by molecular and cellular mechanisms involving both the ischemic and non-ischemic myocardium. The extent of right ventricular (RV) dilatation and dysfunction and its relation to pulmonary hypertension (PH) following AMI are unknown. The aim of the current study was to evaluate changes in dimensions and function of the RV following acute myocardial infarction (AMI) involving the left ventricle (LV).

Methods

We assessed changes in RV dimensions and function 1 week following experimental AMI involving the LV free wall in 10 mice and assessed for LV and RV dimensions and function and for the presence and degree of PH.

Results

RV fractional area change and tricuspidal annular plane systolic excursion significantly declined by 33% (P = 0.021) and 28% (P = 0.001) respectively. Right ventricular systolic pressure measured invasively in the mouse was within the normal values and unchanged following AMI.

Conclusion

AMI involving the LV and sparing the RV induces a significant acute decline in RV systolic function in the absence of pulmonary hypertension in the mouse indicating that RV dysfunction developed independent of changes in RV afterload.