Segmental evaluation of left ventricular wall motion after myocardial infarction: magnetic resonance imaging versus echocardiography.

To assess relative capabilities of magnetic resonance (MR) imaging and two-dimensional echocardiography (2DE) for evaluating regional contractile dysfunction in the left ventricle after a myocardial infarction, results from 22 concurrent MR (orthogonal-transaxial, ECG-gated, multiphasic, single-spin echo) and 2DE examinations were compared. By means of the same 11-segment LV description, MR and 2DE examinations were independently scored segment by segment for residual wall motion (point scores: 2 = normal, 1 = hypokinesia, 0 = akinesia, and -1 = dyskinesia). Significant correlation between MR and 2DE scoring was found throughout most of the left anterior descending (LAD) distribution, but right coronary artery (RCA) distribution (i.e., middle-posterior segment not well seen) could not be fully evaluated by MR imaging. When cumulative scores for the 10 segments mutually evaluated were used to derive measures of global residual LV function (i.e., score quotient [SQ] = accumulated points divided by 20 total possible points), MR SQ correlated well overall with both 2DE SQ (r = 0.82; p less than 0.05) and ejection fraction (EF) from ventriculography (r = 0.86, p less than 0.05 vs r = 0.88, p less than 0.05 for 2DE SQ compared with EF). MR evaluation of segmental wall motion was relatively stronger in the LAD distribution (MR SQ compared with 2DE SQ: r = 0.86, p less than 0.05; MR SQ compared with EF: r = 0.96, p less than 0.05) than in the RCA distribution (r = 0.06, p greater than or equal to 0.05 and r = 0.62, p greater than or equal to 0.05, respectively). For 2DE, regional variations were not as evident (2DE SQ compared with EF: r = 0.90, p less than 0.05 for LAD and r = 0.81, p less than 0.05 for RCA). For segmental evaluation of wall motion after myocardial infarction, MR imaging (transaxial, multiphasic) appears to be comparable to 2DE overall but superior in LAD distribution and inferior in RCA distribution.

MM-CK subtypes diagnose reperfusion early after myocardial infarction.

Isoelectric focusing (IEF) was used to analyze the serum MM-CK isoenzyme subtypes in 16 patients receiving streptokinase (SK) for attempted coronary thrombolysis early after acute myocardial infarction. Twelve patients had revascularization documented by serial coronary angiograms (Group I); in four patients, angiography documented no such reperfusion (Group II). The data also were compared with a previously reported group of 8 patients who did not receive streptokinase (Group III). Total and MB-CK activity, as well as the MM-CK isoenzyme subtypes MM3-CK, MM2-CK, and MM1-CK tended to rise earlier and peak earlier in Group I compared with Group II; serum MM3-CK, the predominant subtype in myocardium, however, definitely peaked earlier in Group I (8.65 +/- 2.07 hr) compared with Group II (18.50 +/- 6.67 hr) (p less than 0.001). Soon after its release from myocardium, MM3-CK is converted in the serum to MM2-CK and eventually to MM1-CK; thus, the MM3-CK:MM1-CK ratio amplifies the time course of subtype conversion. The MM3-CK:MM1-CK activity ratio peaked earlier in Group I (5.51 +/- 0.97 H) compared to Group II (10.74 +/- 3.28 hr) (p less than 0.01), and peaked even earlier than MM3-CK (p less than 0.007) in both Groups I and II. Thus, the time course of the MM3-CK:MM1-CK ratio separates those patients who reperfuse when early SK is used after acute myocardial infarction from those who do not, and does it significantly earlier than the other enzymatic parameters of cellular necrosis, total CK, and MB-CK.

Creatine kinase MM isoenzyme subforms in myocardium, cardiac lymph and blood after coronary artery occlusion in dogs.

A time-varying pattern of creatine kinase MM (CK-MM) isoenzyme subforms has been found in the blood of patients after acute myocardial infarction, but the site of enzyme modification has not been identified. Therefore, we studied the CK-MM subform patterns in myocardium, cardiac lymph and blood of dogs after coronary artery occlusion. In five conscious dogs, serial blood samples were taken for 72 h after occlusion of the left anterior descending coronary artery. Samples of non-infarcted and infarcted myocardium were taken after 72 h. In five other anaesthetised, open-chest dogs, cardiac lymph and blood samples were taken for 6 h after coronary artery occlusion. CK-MM subforms were quantitated by an isoelectric focusing method. Before coronary occlusion, 64% of the total CK activity in blood appeared as the anodal subform CK-MM 1 (pI 6.3); 20% and 9% as the cathodal subforms CK-MM 2 (pI 6.6) and CK-MM 3 (pI 6.9), respectively. However, after 2 h of coronary occlusion CK-MM 2 and CK-MM 3 were increased (38% and 17% of total activity respectively) compared with CK-MM 1. Between 4 h and 10 h, CK-MM 2 and CK-MM 3 decreased as CK-MM 1 increased restoring the control relative activities of subforms. In contrast to the subform changes in blood, CK-MM 3 was the predominant subform in both non-infarcted and infarcted myocardium after 72 h of coronary occlusion and in cardiac lymph during 6 h of coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum creatine kinase MM isoenzyme sub-bands after acute myocardial infarction in man.

Using an isoelectric-focusing (IEF) method developed to quantitate MM isoenzyme-creatine kinase (CK) sub-band activity, we identified a reproducible time-varying pattern of these sub-bands in the serum of eight patients with acute myocardial infarction (MI). Our observations are consistent with the view that MM3-CK (the M2-CK dimer, the pure gene product) is converted intravascularly to MM2-CK, and then to MM1-CK (the M1-CK dimer, the pure postsynthetic sub-band). The MM3-CK reaches a peak first, 16 hours after infarction, followed by MM2-CK, and then by MM1-CK. The MM3-CK is the dominant sub-band in normal myocardium; there is much less MM2-CK and virtually no MM1-CK. The MM3-CK sub-band peak may indicate the time at which enzyme ceases to be released from the injured myocardium. The ratio MM3-CK:MM1-CK rises within 6 hours after onset of chest pain from a baseline of 0.38 and peaks 10 hours after MI. The peak ratio was between 1.1 and 4.2, and the value correlated with the time when total CK activity peaked after MI. The 10-fold change in the MM3:MM1 ratio after MI, as well as the early period at which this ratio peaks (10 hours), makes this an earlier and more sensitive indicator of enzyme release.

Clearance of serum creatine kinase activity.

There is confusion regarding the calculation of serum creatine kinase (CK) activity clearance from an elimination rate constant and a distribution volume derived from one- and two-compartment serum enzyme elimination models. We measured serum CK activity clearance from hepatic enzyme extraction and compared this direct measurement with clearance calculated assuming one- and two-compartment elimination models after bolus and constant infusions of a purified preparation of the MM isoenzyme of CK (MM-CK) activity. Although serum CK activity appears to confer on the body the characteristics of first-order disposition from two compartments, clearance is estimated equally well by one-, two-, and noncompartmental models of disposition and is essentially identical to the hepatic clearance of CK activity. As long as the rate constant and distribution volume are compatible and appropriate for a given elimination model, clearance, the product of the two, will be properly estimated regardless of the model chosen.

Effect of therapy with methylprednisolone on the size of myocardial infarcts in man.

The use of steroids to decrease the size of the infarct and the mortality in patients with acute myocardial infarction has long been the subject of controversy. In the present study, two large doses of methylprednisolone were administered intravenously to 14 patients with relatively uncomplicated myocardial infarction within 17 hours after the onset of symptoms, whereas a comparable group of 15 patients with myocardial infarction served as controls. The size of the infarct was assessed utilizing serial measurements of serum levels of creatine phosphokinase and its myocardial isoenzyme, the MB form of creatine phosphokinase. There was no significant difference between the two groups of patients with regard to peak cumulative levels of total creatine phosphokinase and the MB form of creatine phosphokinase. Similarly, there was no difference between the two groups in mortality or in the incidence of malignant ventricular arrhythmias, atrioventricular block, congestive heart failure, or extensions of the infarct. We conclude that high intravenous doses of steroids given early in the course of myocardial infarction have neither deleterious nor beneficial effects.

Creatine phosphokinase MB isoenzyme in hypothermia: case reports and experimental studies.

Six patients with severe medical disorders and profound hypothermia are presented who had elevated total serum creatine phosphokinase (CPK) and CPK-MB isoenzyme activity without clinical or postmortem evidence of acute myocardial infarction. Experiments in dogs indicate that hypothermia reduces total CPK activity in both striated and myocardial muscle resulting in increased serum enzyme activity. These data suggest that profound hypothermia may result in diffuse striated and cardiac muscle cellular injury without evidence of discrete infarction with consequent release of CPK-MB isoenzyme into serum.

Echocardiographic appearance of ruptured aortic cusp.

Serial echocardiograms of a patient with enterococcal endocarditis and aortic insufficiency suggested the presence of vegetations on the aortic valve with progression of the lesion to frank prolapse of an aortic valve cusp. At surgery, the patient was found to have a flail noncoronary cusp to which an 8 mm vegetation was adherent. Anatomic correlations are presented, and a possible mechanism for the unusual echographic findings is discussed.