Decreased systolic wall thickening in myocardium adjacent to ischemic zones in conscious swine during brief coronary artery occlusion

The purpose of this study was to examine wall thickening in normally perfused myocardium adjacent to acutely ischemic zones. Regional wall thickening (%WT), internal minor axis diameter, and hemodynamics were monitored in nine conscious swine during temporary occlusion of the left circumflex coronary artery (LCCA). Animals were chronically instrumented with ultrasonic dimension gauges for measuring left ventricular (LV) wall thickness and minor axis, catheters in the left atrium and aorta, and a pneumatic occluder around the proximal LCCA. During a 2-minute occlusion of the LCCA, radiolabeled tracer microspheres (10 μm) were injected into the left atrium to determine regional myocardial blood flow (RMBF). Within the ischemic zone, reduction of %WT was related linearly (Y = 24.9 X ?4.1, p < 0.001) to reduced RMBF and endocardial/epicardial blood flow ratio was reduced from 1.30 ± 0.12 (mean ± SE) to 0.87 ± 0.11 (p < 0.01). In zones adjacent to the ischemic zones RMBF was unchanged by LCCA occlusion. RMBF and %WT were poorly correlated (r = 0.38) and endocardial/epicardial blood flow ratio was unchanged from preocclusion values. Therefore, myocardium adjacent to ischemic zones may have reduced thickening despite no apparent blood flow changes. We conclude that such dysfunction may be due to either mechanical tethering effects or a reduction of global LV function due to the presence of an acutely ischemic zone.     

Regional redistribution of myocardial blood flow after coronary occlusion and reperfusion in the conscious dog

Early and late changes in regional myocardial blood flow distribution within the left circumflex coronary arterial bed after occlusion and after occlusion and reperfusion were compared with the extent of myocardial tissue necrosis. Radiolabeled microspheres, 15 μm, were used to study regional myocardial blood flow in conscious dogs at 5 minutes, 2 and 6 hours and 1 month after coronary occlusion. Blood flow was measured in conscious dogs whose hearts were reperfused for 72 hours after 2, 6 and 24 hours of occlusion. Blood flow was measured in four distinct transmural myocardial zones dellneated by dye injections and gross infarct features of the occluded left circumflex coronary bed. After occlusion, myocardial flow was redistributed from deep layers to outer layers, and within 6 hours after occlusion collateral flow was increased to the outer zones in excess of redlstributed flow. After reperfusion, blood flow greatly increased to regions containing predominantly normal tissue, and flow was redlstrlbuted away from the necrotic zones. The indigenous collateral circulation was a major determinant of infarct size in the occluded and reperfused myocardium. The concept of a migrating and narrowing marginal zone is discussed.     

Structural alterations of the porcine heterograft after various durations of implantation

Morphologic changes in six glutaraldehyde-fixed porcine heterografts recovered from five patients were studied with light and scanning electron microscopy. Light microscopy showed minimal changes in the valves recovered after 2 months of implantation. Fibrin deposits, red blood cell trapping, disruption of the valve matrix and interstitial edema were noted in heterografts 2 months and 2 years after implantation. In valves examined with scanning electron microscopy, 6 hours after implantation the surface changes varied from normal to patchy disruptions. Two months after implantation, subendothelial fibers were conspicuous and the geometry of endothellal cells was changed. In valves examined after 6 months in place, many nuclei were burst and fibrin strands were seen over the surfaces. Bacterial infection was observed in two cases. The endothelial cells in the valve implanted for 2 years were completely obscured and some areas were densely covered with fibrillar material where blood cells were trapped in the mesh.     

Relationship between ejection phase indices of performance and myocardial functions during the development of pressure overload hypertrophy

The present study examines the temporal relationship between performance of the hypertrophied nonfalling rabbit heart and the contractility of muscles isolated from these same hearts. Ejection phase indices of ventricular function were determined cineradiographically during the development of hypertrophy. Isolated papillary muscle function was examined an average of 8.6 (early), 40.1 (middle), and 97.5 (late) days after banding of the pulmonary artery. Active tension development at Lmax (F) was depressed by 65% in the muscles examined early and by 43% in the middle group. By the late group, F was comparable to control levels. Early depression and a return to normal function were also observed for peak dF/dt and velocity of shortening at Lmax. Time to peak tension was unchanged at 8.6 days and increased at the middle and late time points. Both percentage of shortening and mean normalized velocity of shortening, determined cineradiographically in the intact heart, were depressed immediately following surgery, gradually returned toward "normal function" by the third week, and plateaued at a stable level of performance, which was maintained thereafter. The similarity of in vivo function of the hypertrophied and control hearts, despite the profound differences observed in the myograph, indicate that "ejection phase indices," such as fiber shortening rate, are poor indicators of intrinsic function during the development of hypertrophy. Moreover, these results demonstrate the extent to which intrinsic functional deficits may be overcome in the whole heart and suggest the presence of mechanisms such as enhanced sympathetic nervous activity, which contribute to the maintenance of this normal basal ventricular function.     

Reduction of exercise-induced ischemic regional myocardial dysfunction by verapamil in conscious dogs

The effects of verapamil on exercise-induced changes in left ventricular (LV) function were examined in nine conscious dogs in which an Ameroid constrictor and Doppler flow probe were placed around the left circumflex coronary artery. Ultrasonic crystals were implanted for measuring LV systolic wall thickness (SWTh) in control and ischemic regions, and a micromanometer measured high fidelity LV pressure. At 23 days (average) postoperatively, coronary collaterals had developed and complete cessation of coronary flow was confirmed by the flowmeter. Control treadmill exercise was then performed for 3.8 minutes at speed 12.1 km/hr and grade 5.3% (average). Two hours after oral administration of verapamil (120 to 160 mg), the same exercise bout was repeated. During the control runs, significant increases occurred in heart rate (101 to 243 bpm), LV end-diastolic pressure (13.3 to 27.5 mm Hg), peak LV pressure (129.8 to 165.7 mm Hg) and its first derivative (3140 to 6275 mm Hg/sec) with an increase of SWTh in control regions, while percent SWTh in ischemic regions decreased markedly (19.6% to 5.9%, p < 0.001); wall thickening velocity also decreased (0.90 to 0.44 SWTh/sec). During the runs after verapamil, the exercise heart rate was significantly lower than in the control run (221 ± 30 bpm), but other hemodynamic measures were similar. SWTh in control regions was unchanged, but exercise-induced dysfunction in the ischemic zone was substantially less (SWTh during exercise 11.5%, p < 0.01 compared to control runs) and wall thickening velocity did not fall. Thus verapamil can reduce regional LV dysfunction produced by exercise in collateral dependent zones, indicating a beneficial effect of this agent on stress-induced ischemia.     

Histologic,ultrastructural, and enzymatic measurements of infarct size following coronary artery stenosis and occlusion

Coronary artery narrowing (CAN), which reduced resting coronary blood flow (BF) by 50%, was induced in 10 conscious dogs and was maintained for 4 hours. Five additional dogs (group 1) with complete coronary artery occlusion were compared to the dogs with CAN. serum isoenzymes of creatine phosphokinase (CK) and latate dehydrogenase (LD) were monitored hourly in all groups. After 36 hours, samples were obtained for regional myocardial BF, quantitative histology, and quantitative ultrastructural (EM) morphology. Six dogs with CAN had small infarcts (MI) of less than 1 gm and persistent myocardial cell injury (group 2). The other four dogs with CAN had only persistent myocardial cell injury by ultrastructural criteria (group 3). Peak serum CK activities in groups 2 and 3 were similar, as were MI sizes calculated from serum CK and myocardial depletion. MB CK was of diagnostic value in group 1 but not in groups 2 and 3. The ratio of $\text{LD}\text{1}\text{LD 2}$ had diagnostic value in all three groups. MI size by enzyme estimates was consistently higher than planimetered MI size at autopsy in both groups 1 and 2. All three groups had significant amounts of ultrastructural damage outside of histologically demonstrated MI. These findings suggest that (1) gross and histologic MI size determination of 36 hours after ischemia underestimate extent of damage, and (2) ultrastructural cell changes cause significant release of CK and LD in coronary disease (CAD).     

Usefulness of the chest x-ray for predicting abnormal left ventricular function after acute myocardial infarction

We evaluated 229 patients discharged after a definite acute myocardial infarction. Pulmonary venous congestion determined from chest x-ray films during the hospitalization and at discharge and the cardiothoracic ratio at discharge were compared to the left ventricular ejection fraction measured at discharge by a gated radionuclide technique. During hospitalization, pulmonary venous congestion was found on at least one x-ray frame in 94 patients (41%). At discharge 134 patients (59%) had abnormal ejection fraction (less than 0.51) and 35 had pulmonary venous congestion (15%). The sensitivity of the x-ray for detecting an abnormal ejection fraction was 20% when pulmonary venous congestion was observed on the discharge x-ray film (specificity 92% and predictive value 77%), 52% if pulmonary venous congestion was present on any x-ray film during the hospitalization (specificity 74% and predictive value 73%), and 47% if the cardiothoracic ratio was abnormal (greater than or equal to 0.50) on the discharge x-ray film (specificity and predictive value 66%). We conclude that an abnormal x-ray film at discharge or during the hospitalization will identify approximately one-half of the abnormal ejection fractions at the time of hospital discharge. Therefore, to reliably assess left ventricular function, either for prognostic or therapeutic purposes in the individual patient, a more direct measure of left ventricular function such as radionuclide angiography must be obtained.     

Cardiac receptors: Their function in health and disease

Cardiac receptors include both mechanically and chemically sensitive receptors located in atria and in ventricles. Atrial receptors innervated by myelinated vagal afferent fibers reflexly regulate heart rate and intravascular volume. On the other hand, stimulation of ventricular receptors can cause either reflex bradycardia and hypotension or, alternatively, excitation of the cardiovascular system. The former response is mediated by vagal afferents, whereas the latter is mediated by sympathetic (spinal) afferents. Under normal circumstances, cardiac receptors sense changes in wall motion or diastolic pressure and perhaps provide a fine tuning of the cardiovascular system. However, under certain pathological conditions such as coronary ischemia, which cause release of substances such as bradykinin and prostaglandins, there is an exaggerated response of the ventricular receptors. Because these receptors cause a reflex depression of the cardiovascular system and, in particular, induce renal vasodilation, they may protect the heart and kidney by lessening myocardial oxygen requirements and by increasing renal blood flow. In the situation of heart failure both atrial and ventricular receptors are reset and therefore provide for an exaggerated neurohumoral discharge. Finally, patients with aortic stenosis may demonstrate a paradoxical vasodilation and syncope during exercise when there likely is excessive stimulation of left ventricular receptors by the high transmural pressure.     

Improvement by propranolol of regional myocardial dysfunction and abnormal coronary flow pattern in conscious dogs with coronary narrowing

The effects of propranolol on regional myocardial function and the pattern of coronary blood flow velocity were studied during partial coronary arterial constriction in conscious resting dogs. Miniature ultrasonic crystals were implanted subendocardially in the left ventricle for measurement of segment length in control and ischemic areas. Coronary blood flow was limited by inflation of an hydraulic-cuff around the left circumflex coronary artery to produce stable hypofunction in the ischemic segment. With coronary stenosis, which reduced mean flow by an average of 31 percent of the control value, the heart rate increased by 17 beats from 78 ± 4 beats/min (mean ± standard error of the mean) and the flow pattern changed from a dominant diastotic to a dominant systolic pattern (peak velocity ratio of systole to diastole, 0.35 ± 0.06 to 1.06 ± 0.09) without change in left ventricular systolic pressure. After administration of propranolol (0.5 mg/kg Intravenously), heart rate decreased to 72 ± 4 from 95 ± 4 beats/min and contraction in the Ischemic segment increased markedly, as did left ventricular wall thickening. Simultaneously, coronary flow returned to a normal velocity pattern. These favorable effects were only partially diminished by cardiac pacing to increase the heart rate to that before treatment with propranolol. This study provides evidence for a substantial beneficial effect of propranolol when myocardial dysfunction results from transient coronary arterial stenosis, and it suggests several mechanisms that may be operative under these conditions.     

Improvement of exercise-induced left ventricular dysfunction with oral propranolol in patients with coronary heart disease.

The effect of propranolol on global cardiac function during exercise was analyzed with equilibrium fadionuclide angiography in 10 patients with ischemic heart disease. All patients had angina pectoris and S-T segment depression of more than 0.1 mv during treadmill exercise when not taking propranolol. Each patient was stressed with supine bicycle exercise to the same work load on a maintenance dose of propranolol (120 to 400 mg/day) and on a second occasion without the drug, the two tests being separated by an average of 16 days. The mean heart rate was reduced both at rest and during exercise after propranolol, but propranolol caused no significant reduction of the left ventricular ejection fraction at rest. In the study without administration of propranolol the average ejection fraction during exercise decreased from 0.56 ± 0.09 (standard deviation) to 0.50 ± 0.14. With propranolol, the ejection fraction was improved from the control value in every patient, the average value during peak exercise reaching 0.60 ± 0.15. Thus, the average ejection fraction increased by 22 percent (±12 percent) relative to the value during the same exercise without propranolol (P < 0.001). In 16 other patients with ischemic heart disease who did not take propranolol, reproducibility of the ejection fraction both at rest and at peak exercise on two occasions within 15 days was good (r = 0.95 and 0.97, respectively). It is concluded that oral propranolol therapy in patients with coronary artery disease can ameliorate left ventricular dysfunction induced by exercise and thereby may reduce myocardial ischemia.     

Cardiac function and myocardial contractility: a perspective

An experimental study was designed to validate postextrasystolic potentiation assessment of myocardial viability or functional reserve of cardiac segments after acute coronary occlusion. Segmental systolic fractional area changes and wall thickening in pacing-induced postextrasystolic beats were mapped in 12 closed chest dogs by two-dimensional echocardiography during a control period and from 20 minutes to 3 hours after occlusion of the left anterior descending coronary artery. The extent of myocardial ischemic and necrotic zones was evaluated in left ventricular slices and subsegements corresponding to echographic cross sections. During two-dimensional echocardiography, left ventricular segments that were found to be neither ischemic nor necrotic always exhibited a significant augmentation of both fractional area change and wall thickening during the postextrasystolic beat that followed an induced premature contraction with a 42.4% coupling interval. In segments without necrosis but with varying degrees of ischemia, significant postextrasystolic potentiation was also demonstrated, even after 3 hours of occlusion. In contrast, segments that developed more than 80% necrosis failed to potentiate systolic fractional area change after 2 hours, and systolic wall thickening, even after 20 minutes of coronary occlusion. Statistical evaluation revealed a characteristic threshold at 41 to 60% necrosis, beyond which no potentiation of function could be elicited 3 hours after occlusion. Extrapolation from the experimental data suggests that when two-dimensional echographic studies in myocardial ischemia indicate postextrasystolic augmentation of segmental left ventricular function, the latter segments may be assumed to contain only small infarcts or to consist of reversibly ischemic and normal myocardium. Conversely, segments that fail to exhibit postextrasystolic potentiation can be assumed to be more than 60% necrotic.     

Left ventricular function in exercise-induced hypertrophy in dogs.

Indexes of left ventricular function and diastolic compliance were studied in 10 awake exercise-trained greyhounds with left ventricular hypertrophy. Mean left ventricular to body weight ratio and mean myocardial cell diameter were significantly greater than in normal dogs (8.73 +/- 2.7 [standard error of the mean] versus 4.63 +/- 0.24 g/kg, P less than 0.01; and 18.3 +/- 0.67 versus 12.5 +/- 0.71 mu, P less than 0.01, respectively). In awake resting animals, 7 to 50 days after implantation of a high fidelity micromanometer and sonomicrometer crystals, left ventricular contractility indexes were similar to those measured previously in normal dogs (maximal derivative of left ventricular pressure [dP/dt] 3,800 +/- 250 versus 3,810 +/- 330 mm Hg/sec, difference not significant; and mean rate of circumferential fiber shortening 1.54 +/- 0.12 versus 1.43 +/- 0.12 sec-1, difference not significant). During volume loading sufficient to produce a left ventricular end-diastolic pressure of 20 mm Hg, changes in contractility indexes were similar to those in normal dogs; however, heart rate increased significantly (74 percent, P less than 0.005) in the trained greyhounds but not in normal dogs. Left ventricular diastolic stiffness did not differ from normal (51.6 +/- 3.0 versus 45.9 +/- 5.9 mm Hg/cm, P less than 0.01). These findings suggest that left ventricular function in exercise-induced left ventricular hypertrophy is substantially normal.     

Usefulness of preoperative and postoperative Tc-99m (Sn)-pyrophosphate scans in patients with ischemic and valvular heart disease.

To assess the usefulness of myocardial imaging with technetium-99m-stannous pyrophosphate for detecting acute myocardial necrosis in patients undergoind cardiac surgery, 66 such patients were stldied. Tc-99m (Sn)-pyrophosphate scans were obtained in all patients 3 to 6 days postoperatively and in 45 preoperatively. Electrocardiograms and serum samples for measuring myocardial isoenzyme of creatine kinase (MB CK) levels were obtained before and serially after cardiac surgery. Seven of the 46 patients undergoing myocardial revascularization had a definite new myocardial infarction as indicated by electrocardiogram and MB CK isoenzyme concentrations, and postoperative pyrophosphate scans were abnormal in all but one. In addition, six of the eight patients with possible myocardial infarction (elevated MB CK levels and persistent ST-T wave depressions) had an abnormal scan postoperatively. Seven of the 20 patients undergoing aortic or mitral valve replacement, or both, had a possible postoperative myocardial infarction by electrocardiogram and MB CK criteria and the myocardial scan was positive in two. All the patients with a normal electrocardiogram and normal MB CK levels had a normal pyrophosphate scan. Preoperative scans were obtained in 22 patients wit; valvular heart disease and were positive in two with a heavy calcified mitral valve on fluoroscopy and in one with a calcified aortic valve. After valve replacement, the pyrophosphate scan became normal in two patients and remained abnormal in the third patient with electrocardiograms and MB CK levels suggesting acute myocardial infarction. We conclude that the Tc-99m (Sn)-pyrophosphate scan is useful for analyzing the occurrence of acute myocardial infarction in patients undergoing cardiac surgery and that, in conjunction with the electrocardiogram, it permits confirmation or exclusion of that diagnosis. Furthermore, false positive pyrophosphate scans may occur in patients with heavy valve calcifications.     

Survival after hospital discharge in matched populations with inferior or anterior myocardial infarction

Prognostic differences between patients with anterior or inferior myocardial infarction are often related to such variables as previous infarction or the size of the myocardial infarct. We examined the determinants of mortality in 997 hospital survivors of acute Q wave infarction (anterior in 449, inferior in 548) who, although not preselected, were well matched with respect to age, sex and prior infarction or congestive heart failure. Additionally, there was no significant difference in peak serum creatine kinase (CK) between the groups with anterior and inferior infarction (1,459 +/- 1,004 versus 1,357 +/- 1,036). Among the patients with anterior infarction who died during the 1 year follow-up period, 56% died in the first 60 days after hospital discharge compared with 18% of those without inferior infarction (p less than 0.01). Survival curves then became nearly identical at 3 months, and remained so until 1 year when the total mortality rate was 10% for the anterior and 7% for the inferior infarction group (p = NS). Variables associated with heart failure during the hospital phase were more prevalent in anterior infarction, but rales above the scapulae during the hospital stay (p less than 0.0001) and ventricular gallop at the time of discharge (p less than 0.0001) were the top two predictors of 1 year mortality by both univariate and multivariate analysis in inferior infarction. Age (p less than 0.0001) and peripheral edema (p less than 0.0001) were the strongest predictors of mortality in anterior infarction. Previous infarction, although just as common in the group with anterior infarction, was present at 1 year in 48% of nonsurvivors of the group with inferior infarction compared with only 19% of survivors (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Interventricular septal motion and left ventricular function after coronary bypass surgery: evaluation with echocardiography and radionuclide angiography.

To evaluate interventricular septal motion and left ventricular function after coronary bypass graft surgery, 40 patients were studied early postoperatively and serially for up to 16 months with echocardiography and radionuclide angiography. Early after operation mean left septal excursion decreased significantly from 4.6 +/- 0.4 (standard error) to 0.8 +/- 0.6 mm (P less than 0.001), and left septal motion was abnormal in 23 of the 40 patients. Mean right septal excursion reversed from 2.1 +/- 0.5 to -2.1 +/- 0.5 mm early after operation in the 22 patients in whom these measurements could be made, and 15 patients showed paradoxical right septal excursion. At a mean of 4 months after operation, only 7 of 35 patients followed up had abnormal left septal motion, and mean left septal excursion had returned toward normal (3.6 +/- 0.7 mm); mean right septal excursion remained reversed (--1.1 +/- 0.7 mm), and 6 of the 14 patients followed up had paradoxical motion. In the 22 patients whose wall thickness could be measured, mean septal thickening during systole decreased significantly from 35 +/- 4 to 21 +/- 3 percent early after operation (P less than 0.01). During late follow-up septal thickening returned toward normal (32 +/- 4 percent). Mean normalized posterior wall velocity increased significantly after operation from 0.76 +/- 0.03 to 1.01 +/- 0.05 sec-1 (P less than 0.001), but posterior wall thickening remained unchanged. Left ventricular end-diastolic dimension and the radionuclide-determined left ventricular ejection fraction were unchanged postoperatively. It is concluded that (1) echocardiographically detected abnormal septal movement is frequent early after coronary bypass graft operation; (2) both decreased myocardial contraction in the septum and increased anterior movement of the whole heart contribute to this abnormality; (3) the abnormalities in septal movement decrease during late follow-up in many patients but persist in some patients; and (4) posterior wall function tends to increase early after operation and therefore overall left ventricular function remains normal.     

Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog: A study based on a modified ultrasonic technique

The thickness of the left ventricular free wall and internal chamber diameter were continuously measured by pairs of ultrasonic crystals together with left ventricular pressure in normal conscious dogs. During the resting state, wall thickness decreased abruptly with the onset of atrial contraction from 10.5 mm to an average end-diastolic value of 9.8 mm. In contrast to most previous studies, there was no change in wall thickness during isovolumic systole, and with ejection the wall thickened by 31.3 percent of end-diastolic wall thickness. Atrial pacing, phenylephrine, isoproterenol and propranolol produced significant changes in chamber size with reciprocal changes in wall thickness. In addition, changes in the extent and velocity of left ventricular chamber shortening in the minor equator were associated with comparable reciprocal changes in the extent and velocity of free wall thickening (correlation coefficients 0.97 to 0.99). During acute coronary occlusion, progressive reductions in the extent and velocity of regional wall shortening with partial ischemia were associated with comparable changes in systolic wall thickening characteristics (r = 0.96 and 0.95), and holosystolic elongation in fully ischemic areas was associated with holosystolic wall thinning. During chronic pressure overload, despite wall thickening, the relation between chamber shortening and wall thickening were retained and direct computation of dynamic wall stress variations was possible. These measurements allowed precise definition of the dynamics of the left ventricular wall during normal and abnormal cardiac states. The demonstration that in the absence of regional dysfunction analysis of wall thickness in a single region of ventricular free wall can be used to describe myocardial and overall left ventricular function, as well as regional function in the presence of ischemia, constitutes a new approach to the assessment of cardiac function that has potential for echocardiographic applications.     

Approach to the estimation of myocardial infarct size by analysis of precordial S-T segment and R wave maps

To assess the correlation of S-T segment elevations and the height of R waves of the precordial electrocardiogram with myocardial infarct size, we performed 35 lead precordial electrocardiograms (maps) in 24 patients with uncomplicated acute anterior transmural myocardial infarction. The initial analysis was carried out in 14 patients. Infarct size was estimated from the integration, from normal baseline to baseline, of serial serum creatine kinase (CK) values obtained at 2 to 4 hour intervals and expressed as IU/liter·hours. The first electrocardiographic maps were recorded 12 hours or less after the onset of symptoms. All S-T segment elevations and R waves were summed for each map (∑S-T and ∑R). There were positive correlations between the ultimate CK infarct size and the initially recorded ∑S-T (r = 0.69), the initially recorded log ∑R (r = ? 0.70) and the initial early decline in log ∑R per hour [(Δlog ∑R/Δhour)·10³, r = 0.88]. Therefore, these variables were combined in a multiple regression analysis; CK infarct size = 0.23 ∑S-T + 0.20 [(Δlog ∑R/Δhour)·10³]? 14.9 log ∑R + 36.8 (r = 0.97). In addition, on the basis of previous studies the initially recorded ∑S-T and log ∑R values were normalized with respect to time by calculating the expected ∑S-T value at 12 hours after the onset of symptoms (∑S-T₁₂) and the 12 hour interpolated values for ∑R (∑R₁₂). These values also showed a good correlation with infarct size: CK infarct size = 0.37 ∑S-T₁₂ + 0.16 [(Δlog ∑R/Δhour)·10³]^t- 18.2 log ∑R₁₂ + 40.4 (r = 0.97).To validate this approach, 10 additional patients were studied prospectively. Correlations between CK infarct size and the various measurements from the serial precordial maps were similar to those in the first study group, and CK infarct size correlated well with the electrocardiographic infarct estimates (r = 0.90 and r = 0.95, respectively). It is concluded that in selected patients CK infarct size can be directly related to the initial height of S-T segment elevations and the early rate of R wave decline and inversely related to later ∑R values, thereby providing a general approach for use in studies on the estimation of myocardial infarct size from precordial electrocardiographic maps.     

Effect of heparin in anticoagulant doses on the electrocardiogram and cardiac enzymes in patients with acute myocardial infarction. A clinical pilot study.

The effect of heparin in clinical anticoagulant doses on S-T segment and cardiac enzymes was studied in 18 patients with acute myocardial infarction by electrocardiogram and enzyme evaluation 1 hour and 24 hours after initial heparin infusion. Intestinal mucosa heparin was given by infusion, 10,000 units after the admission electrocardiogram, and 5,000 units every 6 hours. Data in the nine control and nine treated patients were statistically similar on admission. The electrocardiograph findings were improved, but not significantly, 1 hour after administration of heparin. At 24 hours of heparin therapy, the S-T deviations were reduced 64% (from 139 +/- 2.1 [standard error of the mean] to 50.5 +/- 1.2 mm); in control patients S-T deviations were reduced 21% (from 109 +/- 1.8 to 86 +/- 0.9 mm (t=2.9, P less than 0.019). At 24% hours electrocardiographic leads with 2 mm or more deviation were reduced 86% in heparin-treated patients and 28% in control subjects. Cardiac enzymes were comparably elevated at 24 and 48 hours in both groups, with no clear trend. It is concluded that heparin in anticoagulant doses reduces the 12 lead electrocardiographic pattern of injury without discernibly modifying cardiac enzymes. The question of heparin efficacy in acute myocardial ischemic injury, reopened by findings with large dose heparin in therapy in dogs and anticoagulant dose in this study, awaits further expanded investigation.