Peak Creatine Phosphokinase Research Articles

Role of coronary vasospasm in the pathogenesis of myocardial infarction: Study in patients with no significant coronary stenosis

The role of coronary vasospasm in the pathogenesis of myocardial infarction is unclarified. Among 212 patients with myocardial infarction in whom percutaneous transluminal coronary angioplasty (PTCA) or coronary thrombolysis was not performed at the acute stage, 21 patients (10%) showed no significant coronary stenosis (the degree of stenosis was less than 50% of the luminal diameter) by coronary angiography 4 weeks after myocardial infarction. Among them, 11 (52%) had preinfarction angina at rest, including two with variant angina, and nine (43%) had postinfarction angina at rest. Intracoronary ergonovine maleate induced coronary vasospasm in 12 (75%) of 16 patients examined. Coronary vasospasm occurred in the infarct-related coronary arteries in all patients, and importantly, multivessel coronary vasospasm occurred in 11 patients (69%). The infarct size was relatively small in these patients: (1) seven patients (33%) had Q wave myocardial infarction while 14 patients (67%) had non-Q wave myocardial infarction; (2) peak creatine phosphokinase (CPK) was lower than 1000 IU/ml in all patients; and (3) thallium-201 (TI-201) scintigraphic study showed no perfusion defect in 8 of 18 patients. There was only one patient with congestive heart failure and no patient died. These results suggest that coronary vasospasm may play an important role in the pathogenesis of myocardial infarction in patients without significant coronary stenosis. The relatively small infarct size suggests that coronary reperfusion occurred in the early stages of myocardial infarction.

Age-related variability in the use of cardiovascular imaging procedures.

To determine if older patients undergo fewer cardiovascular imaging procedures (CIPs) than younger patients when admitted to a tertiary care academic medical center for an acute myocardial infarction (MI), after adjusting for disease severity and comorbidities. Non-current prospective cohort study. Urban tertiary care academic medical center. Medical records of 294 patients admitted and diagnosed with an acute MI between January 1990 and April 1991 were reviewed. The total number of different CIPs performed during hospitalization was determined. Cardiac catheterizations, echocardiograms, radionuclide ventriculograms, and thallium scans counted as CIPs. Disease severity was assessed by the Acute Physiology Score (APS) of APACHE II, admission Killip's Classification, and peak creatine phosphokinase (CPK) levels. Comorbidities were assessed using a modified Comorbidity Damage Index of Charlson. The mean (+/- SD) number of different CIPs performed during hospitalization was significantly less for those > or = 75 years old (1.3 +/- 1.0) than for those < 75 years old (1.7 +/- 1.0) (P = 0.01), and CIP number negatively correlated with age (Spearman r = -0.178; P = 0.01). Mean CIP number decreased from 2.0 +/- 1.1 for those < 45 years old to 0.9 +/- 0.6 for those > or = 85 years old (P = 0.02). Other factors positively associated (P < 0.10) with CIP number were: CPK values in the highest quartile of the study population (> 355 U/L); admission to a cardiology, medical, or family practice service; no CIP performed at an outside hospital prior to transfer; admission Killip's Classification of less than IV, and a Q-wave MI. After adjusting for these variables in a multiple regression model, age > or = 75 remained an independent predictor of decreased CIP use (P = 0.003). The modified comorbidity index score and the APS score, a general measure of severity of illness, were not significantly associated with CIP use. When procedures were examined individually, no significant age-related differences were noted in the use of thallium scans, radionuclide ventriculograms, or echocardiograms. Older patients did, however, remain less likely to undergo cardiac catheterizations (P < 0.001). Older patients, regardless of underlying disease severity or comorbidities, undergo fewer invasive cardiovascular evaluations than younger patients when admitted to a tertiary care academic medical center for an acute MI.

Recent changes in the management and outcome of acute closure after percutaneous transluminal coronary angioplasty

The major cause of morbidity and mortality associated with percutaneous transluminal coronary angioplasty (PTCA) is acute closure. This study compared the clinical outcome of 2 groups of patients who experienced acute closure during PTCA. One group was treated during a period when intracoronary stents, laser balloons and perfusion balloons were available for treatment of acute closure (group II). These results were compared with the clinical outcome a group of similar patients who were treated for acute closure during a period that immediately preceded the availability of these devices (group I). One hundred sixty-six patients had acute closure in group I, whereas 156 patients experienced acute closure in group II. Baseline clinical characteristics were similar for both groups. There was no difference in ejection fraction, number of vessels diseased, degree of stenosis or number of vessels attempted between the 2 groups. Patients in group II had more balloon inflations and longer balloon inflation times when compared with patients in group I. Of the 156 patients in group II, 47% were treated with either an intracoronary stent, laser balloon or perfusion balloon. Group II patients had fewer Q-wave myocardial infarctions (9.1 vs 20.3%, p = 0.005). In addition, peak creatine phosphokinase levels (826 ± 1,515 vs 517 ± 1,050, p < 0.01) and mean residual stenosis (40.7 ± 33.2 vs 58.0 ± 34.4%, p < 0.0001) were also lower in group II patients. There was also toss coronary artery bypass grafting during the same admission (38.6 vs 29.5%, p = 0.02) in group II patients. These data suggest that there has been a recent improvement in the clinical outcome of patients with acute closure. This improvement may be related to a more aggressive use of prolonged inflation with standard balloons, in addition to the use of intracoronary stents, laser balloons and perfusion balloons.

Effects of tissue plasminogen activator therapy on the frequency of acute right ventricular myocardial infarction associated with acute left ventricular infarction

To assess the effects of reperfusion therapy on acute right ventricular myocardial infarction, we studied at necropsy the hearts from 51 patients who died after receiving intravenous recombinant tissue plasminogen activator for acute left ventricular myocardial infarction as part of the Thrombolysis in Myocardial Infarction (TIMI) study. Right ventricular infarction occurred in none of 29 patients with infarction of the anterior wall of the left ventricle and in 8 of 22 patients (36%) with infarction of the posterior (inferior) wall of the left ventricle. Of the 22 patients with posterior wall infarction, the 8 patients with right ventricular infarction were compared to the 14 patients without right ventricular infarction. The patients with right ventricular infarction had a longer mean interval from tissue plasminogen activator infusion to peak creatine phosphokinase level (19 vs. 11 h, P < 0.03), a lower frequency of hemorrhagic necrosis (2 of 8 vs. 10 of 14, P < 0.04) and higher frequency of luminal thrombus in the infarct-related coronary artery (6 of 8 vs. 3 of 14, P = 0.054). Each of these findings is associated with the absence of coronary reperfusion. Thus, successful reperfusion following acute left ventricular myocardial infarction appears to be associated with a decreased frequency of concomitant right ventricular myocardial infarction.

Plasma phospholipase A2 activity in clinical acute myocardial infarction.

1. Phospholipase A2 (PLA2) cleaves phospholipids to produce a lyso-phospholipid and free fatty acid and, in view of the biological activity of the products, PLA2 may play a role in many disease states. Lyso-phospholipids and free arachidonic acid increase in ischaemic myocardium, indicating that ischaemia activates the enzyme. 2. Plasma PLA2 activity was measured in patients with acute myocardial infarction, based on the release of labelled arachidonic acid from Escherichia coli cell membrane. Fourteen males (peak serum creatine phosphokinase (CK) above twice upper normal) were studied on day 1 (within 6 h of chest pain onset), days 2-4, and days 6-9. Normal age matched males (n = 13) were also studied. 3. Plasma PLA2 in patients with uncomplicated myocardial infarction (n = 12) was, initially, 1.14 +/- 0.10 (s.e.m.) nmol/min per mL plasma, similar to that in the normal group (1.52 +/- 0.14). On days 2-4, PLA2 activity increased to 1.94 +/- 0.18 (P less than 0.001) and this activity was correlated with the earlier peak CK level (P less than 0.02). On days 6-9, PLA2 activity was 1.49 +/- 0.13 while in two patients who developed complications and underwent open-heart surgery between the last two measurements, there were further increases to 4.22 and 4.04 nmol/min per mL. 4. The increase in plasma PLA2 in uncomplicated myocardial infarction is likely to be due to release from the damaged myocardium; whether it contributes to pathophysiology is uncertain.

Role of creatine phosphokinase in predicting acute renal failure in hypocalcemic exertional heat stroke.

Recruits frequently develop hypocalcemia in exertional heat stroke (ExHS) with rhabdomyolysis and acute renal failure (ARF) from intensive training. It usually indicated severe skeletal muscle damage. However, the relative risk of ARF in ExHS patients complicated with hypocalcemia was unknown. The present study was undertaken to evaluate the value of peak serum creatine phosphokinase (CPK) level in predicting ARF in ExHS patients with hypocalcemia. Sixty-eight army recruits with ExHS were hospitalized at the Tri-Service General Hospital, Taiwan: 17 with ARF and hypocalcemia (group A); 7 with ARF but without hypocalcemia (group B); 20 without ARF but with hypocalcemia (group C); and 24 without ARF or hypocalcemia (group D). In the 24 patients with ARF (groups A and B) the serum phosphate and peak CPK levels were significantly higher than in patients without ARF (groups C and D; p < 0.001), serum calcium levels were also significantly lower in the former (p < 0.001). In the 37 patients with hypocalcemia (groups A and C), the peak serum CPK levels were significantly higher than in those without hypocalcemia (groups B and D; p < 0.001). There was a higher proportion of hypocalcemic patients with peak serum CPK levels greater than 10,000 U/l among ARF compared with patients without ARF (chi 2 = 12.48, p < 0.001). In 24 patients with ARF, there was a negative correlation between serum Ca and peak CPK levels (t = 3.37, r = -0.58, p < 0.01). However, a positive correlation was found between serum creatinine and peak serum CPK levels in 37 patients with hypocalcemia (t = 2.47, r = 0.39, p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Early predictors of smoking cessation after myocardial infarction

The determinants of long-term smoking cessation were evaluated in 80 patients who smoked cigarettes and survived a myocardial infarction. All patients underwent a program of rehabilitation and secondary prevention including in-hospital counseling and physician-guided reinforcing sessions at 1, 3, and 6 months after discharge. At 18 months of follow-up, 53 patients (66.3%) had quit smoking. Variables associated with smoking cessation were duration of hospital stay greater than or equal to 19 days (79 vs. 48%; p less than 0.005) and peak creatine phosphokinase (CPK) elevation greater than or equal to 500 U/l (76 vs. 54%; p less than 0.05). Males tended to quit in higher proportion than females (68 vs. 44%). Age, prior myocardial infarction, other cardiovascular risk factors, infarction location, Killip class at entry, and duration of stay in coronary care unit did not significantly affect the quitting rates. Logistic regression analysis singled out the duration of hospital stay as a significant predictor of smoking cessation (p less than 0.005). Early and intensive secondary prevention during the hospital stay is crucial in promoting sustained smoking cessation after myocardial infarction.

Serial transcardiac lactate netabolism in post-reperfused stunned myocardium in evolving myocardial infarction.

To elucidate the relationship between lactate metabolism following reperfusion and restoration of left ventricular (LV) function, we assessed serial changes in transcardiac lactate metabolism following reperfusion therapy in 67 patients admitted to hospital within 6 h of the onset of acute anteroseptal myocardial infarction. Left ventriculograms taken about 30 min after reperfusion therapy revealed marked dyskinesis in the anteroapical region in all subjects. According to the regional ejection fraction (rEF), determined 4 weeks later as an index of LV function, patients were divided into 3 group: 1) Restored LV group: 28 patients with reperfusion and restored LV function (rEF greater than 30%); 2) Poor LV group: 26 patients with reperfusion but poor LV function (rEF less than 30%); 3) Failure group: 13 patients with failed reperfusion and occluded left anterior descending coronary artery. Although there was no difference in elapsed time and time to peak creatine phosphokinase (CPK) between the former 2 groups, the Restored LV group demonstrated lower peak CPK values, suggesting that these patients had less myocardial injury. Immediately after reperfusion, both groups showed transcardiac lactate production. In the Restored LV group, aerobic lactate metabolism was restored early after reperfusion (at 6 h), while in the Poor LV group prolonged anaerobic lactate metabolism was observed. These results suggest that an early restoration of aerobic metabolism might be a sign of stunned and viable myocardium, and a sustained lactate production might relate to a sustained process of myocardial injury.

Increased arterial adrenaline is related to pain in uncomplicated myocardial infarction

Plasma levels of catecholamines, beta-thromboglobulin (BTG) and arginine vasopressin (AVP), and degree of pain were examined in 22 patients with suspected uncomplicated myocardial infarction within 24 h following onset of chest pain. Sixteen patients developed infarction with peak creatine phosphokinase at 1280 Ul-1 (range 293-3770 Ul-1). Fifteen healthy men served as controls (C). Arterial adrenaline levels were significantly higher in patients with pain (1.15 +/- 0.23 nmol l-1, n = 8, mean value +/- SEM) than in those without pain (0.60 +/- 0.10 nmol l-1, n = 14, P less than 0.05). Plasma catecholamines were moderately but significantly elevated in myocardial infarction; the concentration of arterial adrenaline was 0.83 +/- 0.14 nmol l-1 and that of arterial noradrenaline was 2.70 +/- 0.28 nmol l-1 compared with 0.44 +/- 0.04 nmol l-1 (P less than 0.025) and 1.47 +/- 0.05 nmol l-1 (P less than 0.0005), respectively, in C. One week later, plasma catecholamines had returned to baseline levels. Plasma BTG showed borderline elevation (1.0 +/- 0.1 pmol l-1) compared with C (0.6 +/- 0.1 pmol l-1, P = 0.04), and remained unchanged 1 week later. Plasma AVP was at baseline level. Uncomplicated myocardial infarction, regardless of size, was associated with only moderately increased sympathetic tone. Plasma adrenaline was related more to the degree of pain than to the presence of acute myocardial infarction. Arterial adrenaline may be a sensitive marker of sympatho-adrenal activity related to pain.

Cellular-phase fibrinolysis and coronary reperfusion during acute myocardial infarction: A study in patients receiving intravenous streptokinase-methylprednisoline therapy

Activation of plasma plasminogen to plasmin is the objective of current strategies for thrombolytic therapy. Although thrombolytic activity in blood involves a large cellular component as well as that in plasma, the contribution of this cellular phase to clinical thrombolysis has not been examined. Using a 125I-fibrin test tube assay, we determined blood, plasma and calculated cellular phase fibrinolytic activities in 39 patients with acute myocardial infarction before, immediately after, and at 2 hours after therapy with an intravenous streptokinase-methylprednisolone regimen. By coronary angiography and time to peak creatine phosphokinase levels, 32 patients had coronary reperfusion and 7 did not. Before streptokinase therapy, cellular phase activity of patients who reperfused was more than 2-fold greater than that of patients who did not reperfuse (p < 0.001), while plasma activities were identical, suggesting that intrinsic cellular phase activity may be a determinant of the success of subsequent thrombolytic therapy. In both groups, in addition to the expected (and similar) increases in plasma activity, cellular phase activity increased when compared with pre-treatment values (+96% to +248%; p < 0.001), with accompanying increase in blood granulocyte count (+23% to +65%), indicating that blood cells, as well as plasma, are major contributors to streptokinase-mediated fibrinolysis. Cellular phase stimulation was reproduced in a patient receiving streptokinase without methylprednisolone, and by addition of streptokinase to normal blood in vitro , indicating that streptokinase alone could account for these effects. Increased cellular phase activity in patients who reperfused after streptokinase was similar to that in those who did not reperfuse, when pre-treatment values were considered. These findings indicate that initial cellular phase activity in blood may determine subsequent fibrinolytic response, and that there is a significant cellular phase component to the fibrinolytic response to streptokinase, probably mediated by increased numbers of blood neutrophils, with a possible contribution from increased activity of individual neutrophils.

The complement system in ischemic heart disease.

The mechanisms by which tissue injury after acute myocardial infarction (AMI) occurs has not been fully elucidated. Recent evidence in experimental models has suggested involvement of the complement system in microvascular and macrovascular injury subsequent to AMI. With respect to angina pectoris, whether or not the complement system is activated is not clear. The present study assessed the role of complement as a mediator of myocardial inflammation by quantifying products of complement activation, including C3d, C4d, Bb, and SC5b-9 complexes, in 31 patients with AMI, 17 patients with unstable angina pectoris, 19 patients with stable angina pectoris, and 20 normal volunteers. The plasma C3d levels increased in patients with AMI and in those with unstable angina pectoris (p less than 0.01). The plasma levels of C4d, Bb, and SC5b-9 increased only in patients with AMI (p less than 0.01). The plasma SC5b-9 level was related to peak creatine phosphokinase (r = 0.71) and inversely related to the ejection fraction (r = -0.71). The plasma SC5b-9 level of patients with congestive heart failure was higher than that of patients without congestive heart failure in AMI. These results show that activation of complement system occurs after AMI and show an association of myocardial damage with complement activation. With respect to angina pectoris, the complement system is mildly activated in patients with unstable angina pectoris; however, the cardiac function of patients with unstable angina pectoris is not damaged. The complement system of patients with stable angina pectoris is not activated.

Body surface potential mapping in anterior myocardial infarction--a longitudinal study in acute, convalescent and chronic phases.

Body surface potential mapping (BSPM) was performed to evaluate the infarct size and the viability of myocardium in the infarct area in 20 patients with anterior myocardial infarction (MI). BSPM was performed at the early acute phase, 1 week, 1 month and 2 months after onset of the symptoms. The departure areas were obtained according to the potential distribution below the mean normal range and were compared with the value for creatine phosphokinase (CPK), hemodynamic parameters, ejection fraction measured by radionuclide ventriculography, extent score (ES) and severity score (SS) of thallium-201 single photon emission computed tomogram. Two months after the infarction, the ergometer exercise was performed and departure areas before and after exercise were compared. With the departure map technique, the departure areas in all cases were found in the anterior region of the thorax; From 1 week to 2 months after MI, the departure areas were significantly reduced. One week after MI, the departure areas had a positive significant relation with peak CPK and sigma CPK. One month after MI the departure areas also had a positive relation with ES or SS. One week and 1 month after MI, the departure areas had a negative relation with the left ventricular stroke work index or the left ventricular ejection fraction. After exercise test in the chronic phase, the departure areas were significantly enlarged. In conclusion, the departure map is useful in evaluating the location, sequential changes of size of anterior MI including the ischemic area around the infarct site and the left ventricular function. It is suggested that the enlarged departure areas after exercise might be the ischemic areas provoked by exercise.

Early prediction of left ventricular function in streptokinase-treated acute myocardial infarction.

We administered 750,000 units of intravenous streptokinase to 121 consecutive patients experiencing their first acute myocardial infarction within 4 h of pain onset. The following information was collected: hours between pain onset and streptokinase administration (TS), hours of pain after streptokinase administration (DP), initial and peak creatine phosphokinase levels (ICK and PCK), time to peak creatine phosphokinase, time to electrocardiographic ST segment resolution. Six days after the infarction, catheterization was performed to calculate ejection fraction, infarct-related regional ejection fraction, and dysfunction index. Data was analyzed using stepwise multiple regression. In patients experiencing anterior infarctions, the following equation was obtained predicting the ejection fraction (EF) with a correlation coefficient of 0.86: EF = 69 - 0.0050(PCK) - 3.7(TS) - 1.8(DP). In anterior infarctions the infarct-related ejection fraction and dysfunction index were similarly predictable. We were slightly less accurate in forecasting the outcome of inferior infarctions. The outcome of intravenous streptokinase therapy can be predicted early in the evolution of acute myocardial infarction using routinely available information.

Lack of effect of prior training on subsequent ischaemic and infarcting myocardium and collateral development in dogs with normal hearts.

To determine whether exercise training in animals with normal coronary arteries has a salutary effect on ischaemic myocardium, 24 dogs were randomly assigned to be either trained or confined to cages for three months. All dogs then underwent left thoracotomy for placement of indwelling right and left atrial and aortic catheters and a loose snare ligature around the proximal left circumflex coronary artery. Three days after operation control scintigrams were recorded after injection of thallous chloride-201 in animals running on a treadmill to achieve exercise heart rates of 220 beats.min-1. Four days later the snares were pulled to occlude the left circumflex artery and infarct size determined by measuring venous activity of creatine phosphokinase. Three days after infarction the first post-ligation scintigram was performed after thallium-201 injection in exercising animals. Exercise scans were repeated at 10 days and 2, 4, and 6 weeks after coronary ligation. During the final exercise study collateral blood flow was measured with radioactive microspheres. There was no difference in mean creatine phosphokinase appearance time, peak creatine phosphokinase activity, or measured infarct size between the trained and sedentary dogs. The ratio of thallium-201 activity in left circumflex artery or ischaemic area to left anterior descending artery or normally perfused myocardium fell from 100% before occlusion to 86.6% in the sedentary animals and 80.6% in the trained dogs three days after coronary ligation. Although these falls were significant (p less than 0.025 and p less than 0.005 respectively), there was no difference between groups. Over the next five and a half weeks the scintigraphic defect shrank as the thallium-201 ratio gradually increased, but changes were again similar in both groups. At six weeks there was little difference in exercise collateral flow to left circumflex artery myocardium and flow to normal myocardial tissue in cage confined and trained dogs. Therefore, no beneficial effect of exercise training in dogs with normal hearts could be seen on ischaemic or infarcting myocardium or coronary collateral development after coronary ligation.

Change in Serum Thyroid Hormone Level in Patients with Acute Myocardial Infarction

It has been reported that there is a decrease in the serum concentration of thyroid hormones in non-thyroidal illness. In the present study we made serial measurements of serum concentration of thyroid hormones [triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), reverse triiodothyronine (rT3)], thyroid stimulating hormone (TSH) and thyroxine binding globulin (TBG) in 10 patients with acute myocardial infarction (AMI, Grade I, according to the classification of Killip & Forrester) during 14 days after onset. In the early phase of AMI, serum T3, T4, FT3 and FT4 levels decreased while rT3 increased. TSH and TBG levels, however, were unchanged. In the patients with a high peak creatine phosphokinase activity (greater than or equal to 400 mU/ml), the decrease in thyroid hormone and increase in serum rT3 levels were greater than in patients with a low peak value (less than 400 mU/ml), suggesting a correlation between severity of AMI and changes in serum thyroid hormone levels. Especially, serum FT3 levels fell below the lower limit of controls within 14 days, with the lowest levels and the rT3 peak on the third day after onset. These data suggest that in AMI peripheral conversion of T4 favours rT3 production and that low levels of serum FT3 and T3 protect the infarcted heart muscle against thyroid hormone action.

Comparison of clinical features of non-Q wave and Q wave myocardial infarction

The clinical spectrum and outcome of 119 patients with acute non-Q wave myocardial infarction (NQMI) were studied, in comparison with those of 354 patients with acute Q wave myocardial infarction (QMI). The patients with NQMI had a significantly higher incidence of preinfarction angina (73% vs 63%), previous myocardial infarction (43% vs 22%), multivessel disease (73% vs 51%), postinfarction angina (55% vs 21%), and recurrent myocardial infarction during follow-up for an average of 25 months (17% vs 8%). NQMI patients also had a lower rate of complication of pump fallure and smaller infarct size estimated by peak creatine phosphokinase (CPK) levels (1361 ± 1243 vs 2711 ± 1684 IU/L) than those with QMI. There was no difference in in-hospital mortality between the two groups (17% vs 17%). However, death due to cardiac rupture was exclusively noted in the QMI group. The present study suggests that NQMI is more unstable than QMI in the clinical course.

Right ventricular infarction: Two-dimensional echocardiographic evaluation

Seventeen patients with predominant right ventricular infarction (RVMI) were studied with two-dimensional echocardiography (2DE). On initial 2DE all had abnormal wall motion (AWM), defined as akinesis plus dyskinesis, in the inferior right ventricle (RV), inferior interventricular septum, and inferior left ventricle (LV). The extent of RV vs LV AWM in short-axis sections at mitral, chordal, and papillary levels was 58%·vs 29%, 56% vs 38%, and 59% vs 38%, respectively. The calculated topographic extent of AWM was greater in the RV than in the LV (58% vs 36%, p < 0.05), and the RV LV ratio (1.65) exceeded ( p < 0.001) unity. Peak creatine phosphokinase levels correlated significantly ( p < 0.001) with the topographic extent of LV AWM ( r = 0.79) or RV + LV AWM ( r = 0.75). Although all patients had RV dilatation, eight also had LV dilatation. Serial studies detected the cause of mechanical complications (n = 13), mural echo densities suggesting thrombi (LV in six and RV in seven), and persistent AWM in survivors. Thus, 2DE provided diagnostic data, and assessment of RV and LV AWM confirmed predominant RV involvement.

Prognostic implications of creatine phosphokinase levels after acute myocardial infarction--a study of low risk patients.

To determine the prognostic value of Creatine Phosphokinase (CPK) levels after acute myocardial infarction in patients thought to be at low risk of death or major complications, 94 consecutive patients with definite myocardial infarction were divided into two groups according to peak CPK levels. Group I contained 23 patients with a peak CPK of less than 1000 units and Group II contained 71 patients with a peak CPK level of greater than 1000. They were followed for six months or to death. A CPK of greater than 1000 was significantly associated with left ventricular failure, major arrhythmias and late death and seemed therefore to have value as an indicator of poor prognosis.

Sudden cardiac death: role of left ventricular dysfunction.

Early studies from the Coronary Drug Project of sudden cardiac death in patients surviving an episode of myocardial infarction called attention to the importance of ventricular ectopic beats.' In that study, complex ventricular ectopic beats recorded on a 12-hour Holter electrocardiogram were found to be associated with an excessive risk of sudden cardiac death. When the relationship was examined between complex ventricular ectopic beats and other risk factors, such as age, number of prior infarctions, angina pectoris, hypertension, serum cholesterol, glucose intolerance, cardiomegaly seen on chest X-ray films, and cigarette-smoking, complex ventricular ectopic beats were found to be independent risk factors with respect to sudden cardiac death. The importance of ventricular ectopic beats as a predictor of sudden cardiac death during the convalescent or late hospital phase of acute myocardial infarction in this and other studies has led to the use of prophylactic antiarrhythmic therapy in an attempt to prevent or reduce these ectopic beats and hence to prevent sudden cardiac death. In a subsequent study by Schulze et al. patients surviving an episode of acute myocardial infarction underwent 24-hour Holter electrocardiographic recording and gated radionuclide left ventricular angiography prior to discharge from the hospital.? Several important findings emerged from this study: It was noted that 26 of 29 (90%) patients with complex ventricular arrhythmias (Lown Class 111-V) on Holter electrocardiographic recording had a left ventricular ejection fraction of <40% compared with only 19 of 52 (37%) without complex ventricular arrhythmias. During a mean follow-up period of 7 months, eight patients had documented ventricular fibrillation. All eight patients who suffered sudden death were in the subset of patients with complex late hospital phase ventricular arrhythmias and a left ventricular ejection fraction of <40%. This study was one of the first to call attention to the role of ventricular dysfunction in patients with sudden cardiac death after an episode of acute myocardial infarction. The failure of left ventricular dysfunction to be recognized as an important predictor of sudden death after myocardial infarction in the Coronary Drug Project and in other previous studies may be related to the use of the cardiothoracic (CT) ratio on chest X-ray film as an index of left ventricular function. Subsequent studies have pointed out that the CT ratio is a poor index of left ventricular function and that the correlation between the CT ratio and left ventricular ejection fraction is poor. Schulze et al. also found that the left ventricular ejection fraction and the percent of left ventricular akinesia on gated blood pool imaging were significantly better predictors of subsequent sudden cardiac death than was peak creatine phosphokinase (CPK) determined during the episode of acute infarction. Patients who subsequently died suddenly had

Coronary angiography and left ventriculography in survivors of transmural and nontransmural myocardial infarction

Recent studies have suggested a similar prognosis for patients with transmural myocardial infarction and nontransmural myocardial infarction despite a smaller infarct size in the latter patients estimated by creatine phosphokinase (CPK). Thirty-one patients with transmural myocardial infarction and 17 patients with nontransmural myocardial infarction as defined by electrocardiographic criteria underwent coronary angiography and left ventriculography from 10 to 24 days after they had an acute myocardial infarction. Forty-three of these 48 patients were asymptomatic following their myocardial infarction. When compared to patients with nontransmural myocardial infarction, those with transmural myocardial infarction had greater peak CPK levels, 1,090 ± 210 versus 290 ± 60 IU (p < 0.01). There was no difference in prevalence of single, double or triple vessel coronary artery disease, mean number of coronary arteries 50 per cent narrowed (2.0 ± 0.2 versus 2.0 ± 0.2), near total or total occlusions, coronary score (Friesinger) (7.9 ± 0.6 versus 8.2 ± 0.7), left ventricular ejection fraction (48 ± 2 versus 53 ± 4), or per cent of akinetic-dyskinetic myocardial segments (66 of 242 [27 per cent] versus 32 of 132 [24 per cent]) between two groups. The similar extent of coronary artery narrowing and degree of left ventricular dysfunction may explain the similar prognosis for patients with transmural myocardial infarction and those with nontransmural myocardial infarction despite differences in enzymatically estimated acute infarct size.