Absence Of Infarction Research Articles

Association of severe coronary stenosis with subclinical left ventricular dysfunction in the absence of infarction

Background Regional left ventricular (LV) dysfunction may occur in patients with coronary artery disease (CAD) in the absence of infarction, but the causes of this phenomenon are unclear. We sought to identify whether changes in regional LV function were related to stenosis severity, using sensitive new ultrasound markers of function. Methods We studied 67 individuals with no history of infarction and with normal LV systolic function: 49 patients with CAD and 18 control subjects without CAD. All patients underwent color Doppler tissue imaging, integrated backscatter (IB), anatomic M-mode echocardiography, and strain rate imaging to detect changes in structure and function. Peak early and late diastolic myocardial velocity, cyclic variation of IB, wall thickness, and percent wall thickening were measured in each basal and mid segment. Strain rate and peak systolic strain were calculated in each wall. CAD was defined as ≥50% diameter stenosis. Normokinetic segments (n = 354) subtended by CAD were divided according to stenosis severity into 3 groups: group 1 (subtended by 50%-69% stenosis); group 2 (subtended by 70%-98% stenosis); and group 3 (subtended by ≥99% stenosis). Each parameter in each group was compared with that in 216 segments from control subjects. Results Segments subtended by significant CAD showed lower peak early and late diastolic myocardial velocity compared with control segments. Group 3 showed significantly lower myocardial velocities than group 2 for both peak early (4.8 ± 1.8 vs 6.0 ± 2.0 cm/s, P < .05) and late (4.5 ± 2.1 vs 5.6 ± 2.1 cm/s, P < .05) diastolic myocardial velocity. Group 3 also showed a significantly lower cyclic variation IB than did control segments (6.7 ± 2.3 vs 7.9 ± 2.6 dB, P < .05), but there was no difference in calibrated IB, wall thickness, strain parameters, or percent wall thickening. These differences were not attributable to the distribution of segments for patients with severe CAD, nor were they explained on the basis of collaterals. Conclusion Although the absolute values show overlap between groups, the results of this study indicate that subtle changes of regional LV function may occur in the absence of infarction, in association with severe coronary stenoses.

Can the premises of the spasm of resistance vessel concept permit improvement in the treatment and prevention of ischemic heart disease?

In this communication, the spasm of resistance vessel (S-RV) concept of ischemic heart disease (IHD) and other ischemic will be reviewed and updated, and evidence will be presented that principles of the hypothesis might improve the treatment and prevention of IHD. The S-RV concept provides a different basic pathogenetic framework for IHD, and suggestions for treatment and prevention stem from its different basic conceptualization of this disorder. The concept asserts that S-RV directly induces symptoms in IHD, and this position challenges the accepted pathogenetic mechanism for this disorder, i.e., that symptoms in IHD are due directly to obstructive occlusions of epicardial arteries secondary to coronary artery disease. The S-RV concept avers that ischemia-induced S-RV is a major factor in IHD, and evidence supporting this position is provided. Another major position of the hypothesis is that no-reflow (reduced flow after infarction and severe myocardial ischemia in the absence of infarction) is due to ischemic injury-induced S-RV, and a variety of evidences to support this position are offered. Proposed improvement in the treatment of IHD is based mainly on treating ischemia-induced S-RV. α-Adrenergic sympathetic blockade reverses ischemia-induced S-RV, and α-adrenergic blockade is suggested as therapy for acute coronary syndromes and to prevent complications of percutaneous coronary interventions. Also, angiotensin-converting enzyme inhibition, which has actions similar to α-adrenergic blockade, is also suggested. Proposals for the prevention of IHD are based the prevention of S-RV, and special emphasis is given to preventing exercise- and stress-related IHD.

Brief murine myocardial I/R induces chemokines in a TNF-alpha-independent manner: role of oxygen radicals.

Early chemokine induction in the area at risk of an ischemic-reperfused (I/R) myocardium is first seen in the venular endothelium. Reperfusion is associated with several induction mechanisms including increased extracellular tumor necrosis factor (TNF)-alpha, reactive oxygen intermediate (ROI) species formation, and adhesion of leukocytes to the venular endothelium. To test the hypothesis that chemokine induction in cardiac venules can occur by ROIs in a TNF-alpha-independent manner, and in the absence of leukocyte accumulation, we utilized wild-type (WT) and TNF-alpha double-receptor knockout mice (DKO) in a closed-chest mouse model of myocardial ischemia (15 min) and reperfusion (3 h), in which there is no infarction. We demonstrate that a single brief period of I/R induces significant upregulation of the chemokines macrophage inflammatory protein (MIP) -1 alpha, -1 beta, and -2 at both the mRNA and protein levels. This induction was independent of TNF-alpha, whereas levels of these chemokines were increased in both WT and DKO mice. Chemokine induction was seen predominantly in the endothelium of small veins and was accompanied by nuclear translocation of nuclear factor-kappa B and c-Jun (AP-1) in venular endothelium. Intravenous infusion of the oxygen radical scavenger N-2-mercaptopropionyl glycine (MPG) initiated 15 min before ischemia and maintained throughout reperfusion obviated chemokine induction, but MPG administration after reperfusion had begun had no effect. The results suggest that ROI generation in the reperfused myocardium rapidly induces C-C and C-X-C chemokines in the venular endothelium in the absence of infarction or irreversible cellular injury.

Reperfusion of Specific Brain Regions by Raising Blood Pressure Restores Selective Language Functions in Subacute Stroke

We report a series of six single subject studies examining the effects of pharmacological blood pressure elevation on regional brain perfusion and language function. Previous reports indicate that hypoperfusion of specific brain regions, as delineated by magnetic resonance perfusion weighted imaging (PWI), is associated with disruption of selective lexical functions. On this basis, we hypothesized that reperfusion of the same regions, in the absence of infarct in that region, would restore the associated lexical function. We present five patients with impaired lexical-semantics associated with poor perfusion, but not infarction, of Brodmann's area 22 (BA 22), and one patient with impaired lexical-semantics and a superimposed deficit in retrieving the phonological representations of words, associated with poor perfusion Brodmann's area 37 (BA 37) as well as BA 22. Each patient was treated with induced blood pressure elevation to increase perfusion of the ischemic and dysfunctional tissue. Daily testing of naming and comprehension, with stimulus sets matched for frequency, familiarity, and length, showed improved lexical-semantics in the patients who showed reperfusion of BA 22 and improved oral naming (but not lexical-semantics) in the patient who showed reperfusion of BA 37. These cases illustrate that loss of function with hypoperfusion of a circumscribed area of the brain, and recovery of the same function with improved perfusion of that brain region, can reveal brain/language relationships prior to reorganization after brain injury.

Lessons from experimental models of hibernating myocardium

Chronic animal models of viable dysfunctional myocardium are now available that recapitulate most if not all of the physiological findings in humans with hibernating myocardium. These include chronic reductions in resting perfusion and contractile function, critical limitations in coronary flow reserve and increased uptake of 18F-2-deoxyglucose. These changes occur in the absence of infarction or necrosis and are accompanied by regional reductions in sarcoplasmic reticulum calcium-handling proteins and myocyte loss that arise secondary to apoptosis. Longitudinal studies of viable dysfunctional myocardium indicate that a state of chronic stunning with normal resting flow precedes the development of hibernating myocardium but these are distinct entities within a continuum of chronic adaptations to ischemia. This indicates that reductions in resting flow are the result rather than cause of chronic contractile dysfunction. Thus, the original concept proposing an acute prolonged reduction in flow as the initial stimulus producing hibernating myocardium needs to be revised.

Diffusion-weighted brain magnetic resonance imaging in patients with neurologic complications after cardiac surgery

Introduction. Clinically evident stroke occurs in 2% to 5% of patients after cardiac surgery, but more subtle cerebral ischemia may be missed by computed tomography (CT) or standard magnetic resonance imaging (MRI). Diffusion-weighted MRI (DWI) is more sensitive and specific for acute stroke, and perfusion-weighted MRI (PWI) can demonstrate cerebral perfusion abnormalities in the absence of infarction.

Very low birthweight placenta: clustering of morphologic characteristics.

Our objective was to use factor analysis as a data reduction tool to organize a large number of placental pathologic features into useful aggregates. We examined 1146 placentas of live-born infants with a birth weight of 500-1500 g. We then conducted analyses of pairs of characteristics and multiple characteristics to identify "associated groups" and "factors," respectively. We found an associated group and factor that had placental features associated with acute inflammation and another associated group and factor that had features associated with vasculopathy. Acute umbilical vasculitis had the strongest correlation with other features of the acute inflammation associated group and factor. Gross evidence of acute inflammation (opacification and green appearance of membrane) was eliminated in the reduction from associated group to factor. Infarcts and syncytial knots were strongly dissociated with features of acute inflammation. The multiple pathologic features of the very low birthweight placenta can be aggregated into two associated groups or two factors. Lack of membrane opacification cannot be used as a criterion for declining microscopic examination. The absence of infarcts and syncytial knots should prompt a search for features of acute inflammation. If a placenta has two or more findings from the acute inflammation factor or the vasculopathy factor, it is unlikely to demonstrate features from the other factor.

Nitrate therapy is an alternative to furosemide/morphine therapy in the management of acute cardiogenic pulmonary edema

Background: Nitrates are superior to furosemide in the management of acute pulmonary edema associated with myocardial infarction; however, their role in the absence of infarction is unclear. Methods and Results: A randomized comparison was undertaken of the relative effectiveness of primary therapy with either intravenous morphine/furosemide (men/women; n = 32) or nitroglycerin/ N-acetylcysteine (NTG/NAC; n = 37) in consecutive patients with acute pulmonary edema. The primary end point was change in Pao 2/Fio 2 over the first 60 minutes of therapy. Secondary end points were needed for mechanical respiratory assistance (ie, continuous positive airway pressure via mask or intubation and ventilation) and changes in other gas exchange parameters. Both treatment groups showed improvement in oxygenation after 60 minutes of therapy; however, this reached statistical significance only with NTG/ NAC therapy. There was no significant difference between groups in the assessed parameters (95% Cl for differences in Pao 2/Fio 2: furosemide/morphine −12 to 23 and NTG/NAC 4 to 44), a finding also confirmed in 32 patients presenting with respiratory failure. Only 11% of the study group required mechanical ventilatory assistance (continuous positive airway pressure in 4 patients and intubation and ventilation in 3 patients). Conclusions: NTG/NAC therapy is as effective as furosemide/morphine in the initial management of acute pulmonary edema, regardless of the presence or absence of respiratory failure. The necessity for mechanical ventilatory assistance is infrequent in these patients, regardless of the initial medical treatment regimen.

Immunomodulatory effects of the alkaloid sinomenine in the high responder ACI-to-Lewis cardiac allograft model.

Extracts of the plant Sinomenium acutum have been used safely since ancient times in Chinese medicine for treatment of rheumatic diseases, and the purified alkaloid, sinomenine, was recently shown to have anti-inflammatory and antirheumatic effects. This study describes the effects of sinomenine in the high responder ACI-->Lewis cardiac transplant model in which allograft rejection occurred at 5 days posttransplant. Treatment with sinomenine (15-30 mg/kg/day i.p.) or a subtherapeutic dose of cyclosporine (CsA, 1.5 mg/kg/day, i.m.) prolonged allograft survival only marginally (mean survival of 5.4 and 7.8 days, respectively). In contrast, the combination of sinomenine and CsA had a statistically significant synergistic effect, with a mean survival of 42.2 days (P < 0.001). Allografts harvested at day 5 from recipients treated with either sinomenine or CsA showed dense mononuclear cell infiltrates with widespread subepicardial infarcts, edema, and microvascular platelet and fibrin deposition. Immunohistologic analysis showed that intragraft leukocytes consisted of >75% macrophages with approximately 10-20% T cells and <5% B or NK cells. Mononuclear cell activation was shown by expression of IL-2R (CD25, 10-20%) and labeling for IL-2 (approximately 10%), and IFN-gamma (10-20%), as well as TNF-alpha (>50%) and iNOS (>50%), but only low levels of IL-4 or IL-10 (<5%). Intragraft endothelial cells were activated, as shown by upregulation of MHC class II antigen and ICAM-1 (CD54) compared with only basal levels in normal donors hearts. Combined sinomenine/CsA therapy significantly enhanced graft morphology, resulting in only mild mononuclear cell infiltration, and an absence of infarcts, platelets, or fibrin deposition. Though residual intragraft mononuclear cells at day 5, as in control grafts, consisted primarily of macrophages plus small numbers of IL-2R+ T cells, these cells lacked expression of IL-2, had only low levels of IFN-gamma, but showed dense labeling for IL-4 and IL-10. In addition, TNF-alpha and iNOS were reduced to basal levels and no endothelial cell activation was observed, despite high titers of endothelium-bound IgM, IgG, and C3. Mitogen-induced in vitro proliferation of rat thymocytes was also more effectively decreased by the sinomenine/CsA combination than by either agent alone. These studies demonstrate the therapeutic value of sinomenine in transplantation, and indicate that this agent has novel and interesting antimacrophage, T cell, and endothelial effects that warrant further evaluation.

The risks of thrombolysis in patients without acute myocardial infarction

The risk of administering thrombolysis to patients with suspected myocardial infarction who subsequently do not sustain an infarct, but develop complications associated with thrombolysis is of concern to all physicians. The objective of this study was to ascertain the effect of altering the criteria for the administration of thrombolysis on the number of patients who received thrombolysis in the absence of infarction. During 1990 and 1992 details of all admissions with chest pain were recorded. During 1991 the policy for the administration of thrombolysis was altered so that only patients with ST elevation were eligible. A total of 1473 patients were admitted with chest pain in 1990 and 1967 in 1992. Of the patients admitted in 1990, 663 (45%) had confirmed infarction of whom 378 (57.0%) received thrombolysis. In 1992, 855 (43%) were admitted with infarction and of these 450 (52.6%) had thrombolytic therapy. 118 patients had no evidence of myocardial infarction, but received thrombolysis. 91 (77.1%) were admitted in 1990 and 27 (22.9%) in 1992 ( P < 0.01). Of these only 24 (20%) subjects had ST elevation or bundle branch block on the admission electrocardiograph and 41 (35%) had normal tracings. Four (3%) subjects had serious complications of whom one (0.8%) died. The implementation of ECG criteria resulted in a significant reduction in the number of patients without infarction who received thrombolysis, but did not significantly alter the rate of thrombolysis in those with definite myocardial infarction.

Myocardial Preconditioning: A Model or a Phenomenon?

A brief ischemic episode (ischemic preconditioning) limits myocardial necrosis produced by a prolonged period of coronary artery occlusion and reperfusion. In absence of infarction, lack of cumulative ATP depletion, and ventricular arrhythmias and dysfunction "stunning" in models of intermittent ischemia and reperfusion also could be a component of an adaptive response to brief ischemia (preconditioning). Nonischemic stimuli also precondition the myocardium against ventricular arrhythmias and infarction by activating endogenous mechanism(s) of protection similar to that induced by ischemic preconditioning. Preservation of myocardial ATP, abolishing purine release, attenuation of free radical production, activation of adenosine receptors and KATP channels, and induction of heat shock proteins are common responses to ischemic and nonischemic stimuli of preconditioning. Although a significant reduction in myocardial infarction is critical to myocardial salvage and patient survival, it is equally important to have a functioning heart that can sustain systemic pressure without inotropic support or assist devices. It is scientifically challenging and clinically important to elucidate the mechanisms of myocardial preconditioning. However, it is necessary to expand the definition of myocardial preconditioning to include nonischemic stimuli of preconditioning and other important monitors of myocardial protection such as ventricular function and electrophysiological stability in addition to that of infarction.

Appearance of abnormal Q waves early in the course of acute myocardial infarction: Implications for efficacy of thrombolytic therapy

The purpose of this study was to determine the time course of the appearance of abnormal Q waves on the electrocardiogram (ECG) over the first 6 h of symptoms of myocardial infarction and to determine what implications, if any, such Q waves have for the efficacy of thrombolytic therapy. Severe myocardial ischemia can produce early QRS changes in the absence of infarction. Abnormal Q waves on the baseline ECG may not be an accurate marker of irreversibly injured myocardium. Data from 695 patients who had no past history of myocardial infarction and whose admission ECG allowed prediction of myocardial infarct size in the absence of thrombolytic therapy (Aldrich score) were pooled from four prospective trials of thrombolytic therapy. The presence and number of abnormal Q waves on each patient's initial ECG were recorded. Four hundred thirty-six patients had left ventricular infarct size measured using quantitative thallium-201 tomography a mean (+/- SD) of 52 +/- 43 days after admission. Of patients admitted within 1 h of symptoms, 53% had abnormal Q waves on the initial ECG. Both predicted and final infarct size were larger in patients with abnormal Q waves on the initial ECG independent of the duration of symptoms before therapy (p < 0.001). Despite this finding, the presence of abnormal Q waves on the admission ECG did not eliminate the effect of thrombolytic therapy on reducing final infarct size (p < 0.0001). Abnormal Q waves are a common finding early in the course of acute myocardial infarction. However, there is no evidence that abnormal Q waves are associated with less benefit in terms of reduction of infarct size after thrombolytic therapy.

Cardiac complications of cocaine abuse.

Cardiac complications of cocaine abuse and a rational approach to evaluating and managing them are described. Cardiac abnormalities reported among asymptomatic cocaine abusers include echocardiographic left ventricular hypertrophy and segmental wall motion abnormalities. Electrocardiogram may reveal increased QRS voltage, ST-T changes, and pathologic Q waves. Episodes of ST elevation may be seen during Holter monitoring. The management of cocaine-abusing patients who present to an emergency room with acute chest pain is controversial because the two reported studies yielded conflicting results regarding the incidence of myocardial infarction (MI). Even in the absence of infarction, electrocardiographic abnormalities are common among these patients, which complicates the decision-making regarding hospitalization. Pathophysiology of cocaine-related MI is discussed. Distinct clinical features of cocaine-related MI make it clear that the association between the two is not just temporal. However, considering the number of persons abusing cocaine, it is a rarity. Beta-adrenergic blockers should be avoided in the treatment of cocaine-induced myocardial ischemia which is best treated with nitrates and calcium-channel blockers. Reports of cocaine-induced myocarditis and cardiomyopathy are reviewed. Experimental studies and clinical case reports suggest that cocaine may cause lethal arrhythmias. Cocaine prolongs repolarization by a depressant effect on potassium current and may generate early afterdepolarizations. It is possible that cocaine-associated arrhythmias are secondary to vasospasm-related ischemia and reperfusion as well.

Repeated unilateral carotid occlusion in Mongolian gerbils: quantitative analysis of cortical neuronal loss.

To develop an experimental model which enables quantitative analysis of chronic neuronal loss in the cerebral cortex, repeated ischemic insult was performed using unilateral carotid artery occlusion in Mongolian gerbils. The effect of the time interval between the repeated ischemic insult on the survival rate of the animals and the amount of cortical neuronal loss were examined. The time course of the cortical neuronal damage in repeated ischemic insult was also studied. We repeated the occlusion four times; i.e., one 10-min and three 7-min occlusions (total 31 min of ischemia). The number of animals surviving for 3 weeks after the last ischemic insult was minimum (15.4%) for animals undergoing occlusions at 1-h intervals and maximum (100%) at 24- and 48-h intervals. The number of ischemic neuronal deaths was also dependent upon the time interval, and it was so pronounced as to allow analysis at intervals of 12 hr or 24 hr in the absence of infarction in the cortex. The number of neuronal deaths could not be determined for animals with occlusion at 1-h intervals due to the production of a large infarction, with which the 3-week survival rate was minimum. The temporal profile of cortical neuronal loss in the repeated ischemic insult at 24-h intervals indicated that the number of cortical neurons significantly decreased until 7 days after the start of the ischemic procedure. This model is useful for clarifying the pathophysiology of chronically developing ischemic neuronal death.

Ten-year incidence of myocardial infarction and prognosis after infarction. Department of Veterans Affairs Cooperative Study of Coronary Artery Bypass Surgery.

The 10-year incidence of myocardial infarction (fatal and nonfatal) and the prognosis after infarction were evaluated in 686 patients with stable angina who were randomly assigned to medical or surgical treatment in the Veterans Administration Cooperative Study of Coronary Artery Bypass Surgery. Myocardial infarction was defined by either new Q wave findings or clinical symptoms compatible with myocardial infarction accompanied by serum enzyme elevations with or without electrocardiographic findings. Treatment comparisons were made according to original treatment assignment; 35% of the medical cohort had bypass surgery during the 10-year follow-up period. The overall cumulative infarction rate was somewhat higher in patients assigned to surgery (36%) than in medical patients (31%) (p = 0.13) due to perioperative infarctions (13%) and an accelerated infarction rate after the fifth year of follow-up (average, 2.4%/yr in the surgical group versus 1.4%/yr in the medical group). The 10-year cumulative incidence of death or myocardial infarction was also higher in surgical (54%) than in medical (49%) patients (p = 0.20). According to the Cox model, the estimated risk of death after infarction was 59% lower in surgical than in medical patients (p less than 0.0001). The reduction in postinfarction mortality with surgery was most striking in the first month after the event: 99% in the first month (p less than 0.0001) and 49% subsequently (p less than 0.0001). The estimated risk of death in the absence of infarction was nearly identical regardless of treatment (p = 0.75). Exclusion of perioperative infarctions did not alter the findings. Although surgery does not reduce the incidence of myocardial infarction overall, it does reduce the risk of mortality after infarction, particularly in the first 30 days after the event (fatal infarctions).

Time course of regional function after coronary occlusions of 1- to 120-min duration.

The purpose of this study was to characterize the degree and duration of functional impairment in previously ischemic tissue following coronary artery occlusions of varying duration. Open-chest dogs with left ventricular pressure transducers and ultrasonic segment length crystals were subjected to coronary artery occlusions of 1 (n = 22), 5 (n = 8), 10 (n = 7), 15 (n = 8), 20 (n = 7), 30 (n = 6), 60 (n = 10), or 120 (n = 8) min and segment length motion was measured during 6 h of reperfusion. Active shortening was replaced by passive lengthening during coronary occlusion and regional myocardial blood flow within the ischemic zone was always less than 0.4 ml . min-1 . g-1. Following reperfusion, the improvement of ischemic segment length function was inversely proportional to the duration of coronary occlusion. Function in previously ischemic segment lengths recovered rapidly after 1- and 5-min coronary occlusions, but after occlusions of 10-20 min, there was slow, though incomplete, return of some degree of active shortening yet no evidence of myocardial infarction. With occlusions exceeding 20 min there was persistence of systolic passive lengthening for 6 h despite the absence of infarction in the segment lengths in which function was being evaluated, although infarcted tissue was present ranging from 16.5 +/- 2.6% of the area of ischemia in dogs with 60-min coronary occlusions to 37.2 +/- 4.6% of the area of ischemia in dogs with 120-min occlusions.

Thallium-201 myocardial redistribution imaging 24 hours following stress exercise.

Twenty-four-hour 201-thallium chloride redistribution images in conjunction with immediate postexercise images were evaluated to determine their value in distinguishing coronary artery ischemia from remote infarction. Cardiac angiography, including selective right and left coronary angiography and left ventriculography, was also performed. For 43 patients with a prevalence of coronary artery disease of 0.58, 24-hour redistribution images indicated the presence of remote infraction with a predictive value of 0.75 and the absence of infarction with a predictive value of 0.92. Twenty-four-hour redistribution images are considered to be clinically efficacious, convenient for scheduling purposes, and useful as an alternative to other redistribution intervals.

Pyrophosphate myocardial imaging

Technetium-99m pyrophosphate myocardial scintigraphy is a sensitive indicator of acute myocardial infarction (AMI). Over 90% of acute myocardial infarctions will result in an abnormal scintigram. The sensitivity is highest for transmural myocardial infarction, reaching levels of 95% or better. The positivity rate for subendocardial infarction ranges from 40% to 88% depending on the criteria used for interpreting the study. The threshold for positivity may be established using the intensity level present within the myocardium, on the presence or absence of localization within a specific wall of the myocardium, or a combination of both. The more stringent the criteria and the higher the threshold for positivity, the greater will be the specificity for acute infarction. The high specificity will, however, be at the expense of a lower sensitivity. Several other pathologic conditions can yield a positive myocardial scintiphotogram. Most commonly these are other forms of coronary artery disease in which frank myocardial infarction is not occurring. The cause of positive scintiphotograms in the absence of acute myocardial infarction is not known. It may be that with ischemia there are small focal areas of necrosis or that pyrophosphate concentration occurs purely on the basis of the ischemia. In the absence of infarction, the pattern of positivity is usually diffuse rather than localized in a specific wall. There are exceptions to this, most notably with ventricular aneurysms; however, the presence of a localized abnormality generally increases the specificity of a positive scintiphotogram for AMI. A positive scintigram in the absence of acute infarction has prognostic value in coronary artery disease for some conditions. A persistently positive study following a remote infarction is associated with an increased morbidity and mortality. Likewise, a positive scintiphotogram before coronary artery bypass surgery portends a higher surgical risk. Other indications for the examination include the diagnosis of perioperative infarction and right ventricular infarction. Less common entities such as metastasis to the myocardium, myocardial trauma, radiation therapy, or any other entity leading to significant myocardial injury or cellular death may result in an abnormal scintiphotogram.

Evaluation of radioactive potassium and its analogues for imaging myocardial infarcts

An extensive clinical evaluation was undertaken to assess the value of myocardial infarct imaging with radioactive potassium and analogues. Of 130 patients so examined, 80 were diagnosed as having suffered infarcts in the recent or distant past on the basis of all information other than the scan. The radionuclide imaging results were abnormal in 87.5% overall, 97% in acute transmural infarcts, and 83% in lesions over 3 weeks old. In 50 patients not considered to have had myocardial infarcts or contusions, apparently false abnormal results were obtained in 15%. These were all patients in whom additional diagnostic help was desired after the ordinary laboratory tests and electrocardiograms. Excellent agreement of infarct location was discovered on comparing radionuclide scans with radiographic contrast ventriculography. On comparing electrocardiograms with scans for infarct location, 85% complete or partial correlation was revealed. Agreement between scan abnormalities and significant-appearing coronary arteriographic lesions was rather poor, causing one to realize that 43K scan abnormalities indicate regions of poor blood extraction by old or recent infarcts, rather than just poor regional arterial perfusion. While costly, radionuclide scans often provide worthwhile information about presence or absence of infarcts as well as about their location and size. Electrocardiograms and blood enzyme levels each cost less, but are almost always performed in serial fashion. This makes them actually more expensive than a single scan. Furthermore, a normal scan in a patient being considered for acute coronary care may be used as potent argument against the presence of an infarct, thereby saving costly intensive care and monitoring.

Left-axis deviation: etiologic factors in one-hundred patients

Clinical and electrocardiographic findings were analyzed in 100 consecutive cases of LAD. Below the age of forty years, LAD was uncommon, but its incidence increased continuously thereafter. The most frequent primary clinical diagnosis was arteriosclerotic heart disease. The functional mechanism producing LAD most often was LAHB, responsible in about 40 per cent. Approximately half the instances of LAHB were associated with old myocardial infarction of septal, anterior, or lateral regions, but half were seen in the absence of infarction or clinical coronary sclerosis and are presumed due to primary degenerative processes within these specialized conducting fibers. Approximately one-sixth of the instances of LAD were due to loss of inferior forces following inferior myocardial infarction. Typical left ventricular hypertrophy was a distinctly uncommon cause of LAD. Last, in 24 patients with LAD the mechanism or cause was not evident initially, of which two were subsequently shown to represent a very mild degree of LAHB. Also it is suggested that asymmetric myocardial hypertrophy of the anterior wall may account for some instances of LAD not otherwise explained.