Early Phase Of Acute Infarction Research Articles

Left ventricular dysfunction in ischemic heart disease: Fundamental importance of the fibrous matrix

The contractile function of the myocardium is coordinated by a fibrous matrix of exquisite organization and complexity. In the normal heart, and apparently in physiological hypertrophy, this matrix is submicroscopic. In pathological states changes are frequent, and usually progressive. Thickening of the many elements of the fine structure is due to an increased synthesis of Type I collagen, This change, which affects the myocardium in a global manner, can be observed by light microscopy using special techniques. Perivascular fibrosis, with an increase in vascular smooth muscle, is accompanied by development of fibrous septa, with a decrease in diastolic compliance. These structural changes are believed to be due to increased activation of the renin-angiotensin-aldosterone system, and to be independent of the processes of myocyte hypertrophy. Reparative or replacement fibrosis is a separate process by means of which small and large areas of necrosis heal, with the development of coarse collagen structures, which lack a specific organizational pattern. Regarding ischemic heart disease, an increase in tissue collagenase is found in experimental myocardial "stunning" and in the very early phase of acute infarction. Absence of elements of the fibrous matrix allow for myocyte slippage, and--if the affected area is large--cardiac dilatation. If, subsequently, the necrosis becomes transmural, there is further disturbance of collagen due to both mechanical strain and continued autolysis, During healing collagen synthesis increases greatly to allow for reparative scarring in the available tissue matrix. In cases of infarction with moderate or severe initial dilatation, pathological hypertrophy of the spared myocardium is progressive, accounting for late heart failure and poor survival.(ABSTRACT TRUNCATED AT 250 WORDS)

CORONARY ANGIOPLASTY IN THE REPERFUSION ERA.

We have entered the reperfusion era for the treatment of acute myocardial infarction: intravenous thrombolysis is rapidly becoming standard care for the early phases of acute infarction. Where does …

Anterior ST-Segment Depression Associated with Acute Inferior Myocardial Infarction: Clinical, Hemodynamic, and Angiographic Correlates

Clinical, hemodynamic, and angiographic data were analyzed in relation to the presence or absence of anterior (I, aVL, and V(1(1–6)) electrocardiographic ST-segment depression in 21 patients with acute inferior myocardial infarction. All data were obtained within 12 h of onset of chest pain. Greater than 1 mm anterior ST-segment depression was frequent (19 of 21 patients) during the early phase of acute infarction. There was a significant correlation between the single electrocardiographic lead with the greatest inferior ST-segment elevation and the single anterior lead with the greatest ST-segment depression (r = 0.87, p < 0.001), and between the sum of STsegment elevation in the inferior leads and the sum of ST-segment depression in the anterior leads (r = 0.77, p < 0.001). The patients with >2 mm anterior ST-segment depression had a higher left ventricular end-diastolic pressure than those with ≤2 mm ST-segment depression (18.4 vs. 10.8 mm Hg, p < 0.01) only when leads I and aVL were included, but there were no clinical, angiographic,or other hemodynamic differences between the groups. These findings do not correlate anterior ST-segment depression associated with inferior myocardial infarction with a higher cardiovascular risk with regard to the variables examined.

Myocardial scintigraphy with technetium-99m pyrophosphate during the early phase of acute infarction

To determine the sensitivity of myocardial scintigraphy with techne-tium-99m pyrophosphate during the early phase of acute myocardial infarction, 31 patients admitted to the coronary care unit with prolonged ischemic pain underwent imaging within 4 to 8 hours and again at 24 hours after the onset of symptoms. In 11 of 15 patients with documented acute myocardial infarction, increased focal myocardial uptake was demonstrated on early myocardial scintigraphy. Focal uptake was observed in only 2 of 16 patients with unstable angina pectoris. Three of four patients with normal early scintigrams had massive transmural myocardial infarction. Normal early scintigrams in these three patients may have reflected poor perfusion because the images were abnormal at 24 hours. In four patients the extent of technetium-99m pyrophosphate uptake increased more than 20 percent at 24 hours without other evidence of infarct extension. In the other seven patients, there was no significant change in the area of the abnormal radioactive uptake between early and delayed scintiscans. This study suggests that technetium-99m pyrophosphate scintigraphy can detect acute myocardial infarction as early as 4 hours after the onset of symptoms although the sensitivity rate (73 percent) is less than that at 24 hours.

Loss of electrically active myocardium during anterior infarction in man.

A method has been developed of praecordial mapping of changes in R/S ratio and the appearance of Q waves in acute myocardial infarction. Observation of the serial changes in R and Q waves in 40 patients with uncomplicated anterior infarction shows that the loss of electrically active myocardium occurs within 6 hours of the onset of chest pain. Complications, such as recurrent chest pain, associated with extension of myocardial necrosis can be identified and assessed. The total praecordial changes in R/S ratio and Q wave amplitude correlate with the total MB fraction of creatine kinase activity released into the plasma in 20 patients after uncomplicated anterior infarction. This technique for identifying those factors that may modify the progressive loss of active myocardium in the early phase of acute infarction of the heart is noninvasive and repeatable.

Effects of intravenously administered digoxin on mild left ventricular failure in acute myocardial infarction in man

Studies were made in 10 patients with early mild left ventricular failure in acute myocardial infarction to determine the hemodynamic correlates of the condition and evaluate the effects of intravenously administered digoxin. Studies were performed within 72 hours of infarction. Patients with basilar rales, tachycardia and ventricular (S 3) gallop sound were selected for study. Findings during the control period were consistent with mild left ventricular failure. Stroke index was below normal (28 ± 7.1 ml/m 2), but cardiac index was within normal limits (3.22 ± 0.60 liters/min per m 2) because of tachycardia. Stroke work index was low (39 +- 13.7 g-m/m 2), and pulmonary arterial end-diastolic pressure was minimally increased (15.2 ± 3.5 mm Hg). After intravenous administration of digoxin (0.75 mg in 7 patients, 1.0 mg in 3 patients), there were no statistically significant changes in any of the measured variables when the whole group was considered. Relating stroke work index to pulmonary arterial diastolic pressure, 2 types of responses were found. Four patients had a distinct inotropic response; the other 6 patients had no significant change, or a worsening of function. The reasons for a variable response in the early phase of infarction may be related to the regional nature of infarction or possibly to humoral factors influencing myocardial performance. Data suggest that digitalis is of limited value during this stage of infarction. Further studies and more precise characterization of patients may provide insight into the role of digitalis in the early phases of acute infarction.