LCX Occlusion Research Articles

Regional myocardial contractile response to the beta-adrenergic stimulant prenalterol in the conscious dog following myocardial infarction. Mechanism of hemodynamic effect.

In order to assess regional myocardial contractile responses to the beta-adrenergic stimulant prenalterol after recent myocardial infarction, 9 male mongrel dogs underwent left circumflex coronary artery (LCX) occlusion after implantation of miniature subendocardial sonomicrometer crystals in normal, marginally ischemic (border) and central ischemic zones. 90-min LCX occlusion with reperfusion resulted in substantial infarction (mean +/- SEM 24 +/- 3% of total left ventricular area) and characteristic regional functional alterations. In conscious, unsedated animals 72 h after infarction, intravenous prenalterol (30 micrograms/kg) significantly decreased end-diastolic and end-systolic segment length and increased percent systolic shortening in normal and border zones, but did not alter ischemic zone function. Heart rate increased significantly with prenalterol. Regional myocardial function before drug administration correlated closely with response to the inotropic agent. These results indicate that the mechanism by which prenalterol improves cardiac function 72 h after myocardial infarction is stimulation of normal and marginally ischemic myocardium.

The effect of ibuprofen on accumulation of indium-111-labeled platelets and leukocytes in experimental myocardial infarction.

To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 (111-In)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occlusion) by 40%, from 48 +/- 4% in control animals to 29 +/- 4% in ibuprofen-treated dogs (p = 0.005). Quantification of the platelet-associated 111In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.41-0.60 gram infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2 in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes accumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction.

Regional dysfunction of the interventircular septum during acute coronary artery occlusion.

To compare the effects of local myocardial ischaemia on the dynamics of different portions of the interventricular septum (IVS), pairs of miniature ultrasonic crystals were implanted across the anterior and posterior portion of the IVS and the left ventricular free wall (LVFW) to measure wall thickness changes in open chest dogs. Following left anterior descending coronary artery (LAD) occlusion, the end-diastolic wall thickness decreased in all areas indicating significant chamber dilation. Systolic thickening was reduced from 19.2% to 0.8% in the anterior LVFW and from 16.0% to 4.1% in the anterior IVS, while a significant increase in thickening occurred in the posterior LVFW (from 17.1% to 21.0%) and in the posterior IVS (from 13.6% to 16.5%). Left circumflex artery (LCx) occlusion produced a greater distension of the ischaemic free wall and the magnitude of responses tended to be less in the IVS than in the free wall (percentage thickening being reduced from 15.3% to 7.2% in the posterior IVS, and from 17.4% to -4.4% in the posterior LVFW). Enhancement of the systolic thickening of the normal perfused area was more marked with LCx occlusion than with LAD occlusion. Percentage thickening increased from 19.0% to 26.9% in the anterior LVFW and from 17.2% to 28.6% in the anterior IVS. These findings indicate that the ischaemic responses of the IVS, as induced by ischaemia differed in the anterior and posterior portion of the septum. Thus, when attempting to assess clinical echocardiographic findings of an ischaemic septum, one should take into account these regional differences with regard to which area of the septum the ultrasonic beam had passed.

Effects of propranolol on myocardial infarct size with and without coronary artery reperfusion in the dog.

The ability of propranolol to limit myocardial infarct size (IS) following coronary artery occlusion with and without reperfusion into a critical stenosis was assessed in the dog. IS was determined by the nitrobluetetrazolium staining method and expressed as percent of the left ventricle (free wall plus septum). In Series 1 dogs the left circumflex coronary artery (LCX) was ligated at its origin. IS at 6 h was similar in groups pretreated with saline (36.0 +/- 1.3%) or propranolol (0.2 mg . kg-1, 34.7 +/- 1.7%; 1.0 mg . kg-1, 36.7 +/- 1.5%; 4.4 mg . kg-1, 34.8 +/- 0.3%). In Series 2 dogs a relatively small infarction was produced by ligating the largest branch of the LCX between the left anterior descending and posterior descending arteries. IS at 6 h was not significantly different in dogs pretreated with saline (8.1 +/- 1.7%) or propranolol (0.2 mg . kg-1, 7.1 +/- 2.5%; 1.0 mg . kg-1, 4.6 +/- 1.2%). In Series 3 dogs the LCX was ligated approximately 10 mm from its origin for 60 min followed by reperfusion into a critical stenosis. IS determined at 24 h was significantly less in dogs treated with propranolol (1.0 mg . kg-1) before LCX occlusion (4.6 +/- 0.6%) or 5 min after LCX reperfusion (9.5 +/- 1.8%) than in dogs treated with saline (22.6 +/- 2.8%). In Series 4 dogs treatment was exactly as in Series 3 except that reperfusion was not instituted. IS was similar in dogs pretreated with saline (29.0 +/- 1.5%) or propranolol (31.1 +/- 3.0%). Thus, in the present study, propranolol limited IS in the presence but not in the absence of reperfusion. In the reperfusion model propranolol was effective when administered before coronary occlusion or after initiation of reperfusion.

Effect of graded coronary constriction on the flow reserve in regional myocardium in dog.

Effects of coronary constriction on the flow reserve of regional myocardium were studied in the anesthetized open-chest dogs. Regional myocardial blood flow (RMBF) was continuously measured using heated crossthermocouple method. Left circumflex coronary artery (LCX) was constricted gradually with a screw type constrictor. The coronary constriction decreased subendocardial myocardial blood flow, while subepicardial myocardial blood flow was not affected until reactive hyperemia in LCX nearly disappeared. Recovery and arrival to peak flow rate of RMBF following the release of 15-second's occlusion of LCX were progressively delayed with an increase in the constriction, especially in the subendocardial myocardium. Repayment of flow debt, however, was remained relatively well since the duration of reactive hyperemia in RMBF was prolonged by an increment of the constriction. From these findings, it might be concluded that in the heart with coronary stenosis recovery from ischemia was caused by prolonged duration of reactive hyperemia, and is suggested that the time required for recovery from ischemia or ischemic abnormalities after the cessation of stress might be an important marker for the severity of coronary insufficiency.

Inability of methylprednisolone sodium succinate to decrease infarct size or preserve enzyme activity measured 24 hours after coronary occlusion in the dog.

Methylprednisolone sodium succinate (50 mg/kg) was given 30 minutes before or after the start of a 90 minute occlusion of the left circumflex coronary artery (LCX) in one group of dogs. In a second group, methylprednisolone sodium succinate was given 15 minutes after permanent occlusion of the left anterior descending artery (LAD). Infarct size was determined by dehydrogenase staining after 24 or 96 hours. Heart slices were incubated with nitro-blue tetrazolium and nonstaining infarcted tissue was dissected and weighed. Myocardial depletion of creatine phosphokinase activity (CPK) and lactate dehydrogenase activity (LDH) were determined 24 hours after temporary LCX occlusion. When measured after 24 hours, methylprednisolone sodium succinate treatment did not reduce infarct size or decrease enzyme loss. After temporary LCX occlusion infarct size was 30.4 +/- 3.6% of left ventricular weight in control dogs and 30.0 +/- 2.3% in treated dogs. No significant difference in infarct size was observed in hearts examined 24 or 96 hours after myocardial infarction. After permanent LAD occlusion, infarct size in control dogs was 39.2 +/- 1.6% of left ventricular weight and 33.7 +/- 3.5% in treated dogs. CPK activity in the LCX area decreased by 26.5 +/- 7% in controls and by 28.1% +/- 7% in treated dogs. Treated dogs sustained a significantly greater fall in arterial blood pressure after LCX occlusion than did controls. During LCX occlusion and upon reperfusion, methylprednisolone sodium succinate treated dogs exhibited a significantly greater number of premature ventricular beats. Since infarct size and enzyme depletion were not reduced when measured after 24 hours, methylprednisolone sodium succinate treatment does not appear to have enhanced myocardial cell viability.

Prediction of the Site of Coronary Artery Lesion in Acute Inferior Myocardial Infarction with Right Sided Precordial Lead (V4r)

Background: The patient with inferior wall AMI, site of culprit lesions is an important determinant of outcome. Patient with RV infarction have a poor prognosis whereas those with occlusion of LCX have a good prognosis. Early diagnosis and treatment substantially reduce cardiac events particularly in high-risk patients. V4R can be used as to locate the site of obstruction. Materials and methods: 81 patients with acute inferior myocardial infarction admitted to the coronary care unit (CCU) within 12 hours after the onset of chest pain who underwent coronary angiogram were included in the study. Standard 12-lead ECG with right precordial lead V4R was recorded. Patients were categorized into within 3 groups according to early changes of V4R-Group- I - ST-segment elevation > 1 mm and positive T- wave, Group-II- ST-segment iso-electric and positive T-wave, Group-III- ST-segment depression >1 mm and negative T -wave. Results: In group I patients, highest percentage of the patients had lesion in proximal RCA (97.2%); whereas in group II patients, highest percentage in the distal RCA (89.7%) followed by LCX (41.4%) and in group III patients, highest percentage also in LCX (100.0%) followed by LAD (56.3%). Based on analysis of sensitivity and specificity, it was revealed that in group I patients of ECG finding suggested 100.0% sensitivity, 97.8% specificity and 98.8% accuracy. In group II patients, 92.9% sensitivity, 94.3% specificity and 93.8% had accuracy. In case of group III patients, 93.8% sensitivity, 98.5% specificity and 97.5% accuracy. Conclusion: The configuration of the ST-T segment in lead V4R is a sensitive and specific tool to recognize the occluded vessel in acute inferior MI whether it is proximal RCA, distal RCA or LCX. Since it is an inexpensive method, it can be readily used to locate the site of occlusion in AMI - Inferior. Keywords: Coronary artery disease; Myocardial infarction;, Lead V4r. DOI: http://dx.doi.org/10.3329/cardio.v4i1.9389 Cardiovasc. J. 2011; 4(1): 46-52