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K A Reimer

Publications and source records attributed to K A Reimer.

At least 37 records · Page 2Linked to original sources
PubMed1994

Magnetic resonance imaging of chronic myocardial infarcts in formalin-fixed human autopsy hearts.

BACKGROUND: In post-myocardial infarction patients, three-dimensional structure of the infarct as well as infarct size are likely to be important factors affecting mortality, cardiac function, and arrhythmias. Current morphological methods for determining three-dimensional infarct structure in autopsied hearts are inexact and time consuming. The cardiac magnetic resonance imaging techniques used in living patients have shown potential in determining infarct size and structure but have limited resolution for morphometric postmortem studies. The recent development of magnetic resonance microscopy raises the possibility that three-dimensional infarct structure can be quantified at microscopic levels in autopsied hearts. The purpose of this study was to determine the ability of magnetic resonance imaging at different spatial resolutions to differentiate infarcted from noninfarcted myocardium. METHODS AND RESULTS: Magnetic resonance imaging was performed at 2.0 T on cross sections taken from 10 autopsied hearts containing old myocardial infarcts. T1 was derived from six images with repetition times (TRs) for each image ranging from 100 to 3200 milliseconds. T2 was derived from multi-echo images with echo times (TEs) ranging from 10 to 60 milliseconds. Resolution was approximately 400 x 400 microns in 2-mm-thick slices. Sites of infarcted and noninfarcted tissue were identified from histological sections taken from each slice, and the T1 and T2 values of these sites were obtained. Microscopic images were acquired with voxels of 100 x 100 x 625 microns, representing tissue volumes more than 1000-fold smaller than conventional clinical images. In all cases, T1 of infarcted tissue (459 +/- 266 milliseconds, mean +/- SD) was greater than that of noninfarcted tissue (272 +/- 163 milliseconds). Also, in all cases, T2 of infarcted tissue (49 +/- 14 milliseconds) was greater than that of noninfarcted tissue (35 +/- 8 milliseconds). CONCLUSIONS: T1 and T2 values for infarcted tissue are significantly different from those of noninfarcted tissue (P < .001). Based on these findings, it should be possible to develop techniques to perform three-dimensional imaging and quantitation of infarcts with a resolution of 400 microns or less. When volumetric three-dimensional imaging was performed using a T1-weighted sequence, the resulting 256(3) arrays supported isotropic resolution at 400 microns (voxel volume, 0.064 mm3). Subsequent volume rendering using a compositing algorithm clearly shows the infarcted areas in three dimensions. The techniques demonstrate the potential for quantitative three-dimensional cardiac morphometry using magnetic resonance imaging.

Algorithms↗
PubMed1994

Acute myocardial ischemia: effects of reperfusion with arterial blood.

Periods of severe ischemia of 15 minutes or less injure myocytes of the dog heart reversibly in that reperfusion of the affected tissue with arterial blood salvages all myocytes destined to die if the ischemia is not relieved. While the myocytes are ischemic, they develop numerous changes as a consequence of ischemic metabolism including depletion of approximately P and accumulation of glycolytic intermediates, H+, and the end-products of adenine nucleotide pool degradation. With restoration of arterial flow, aerobic respiration resumes. Lactate and other intermediates are reutilized or are washed to the systemic circulation. If the period of severe ischemia is extended to 40-60 minutes, the injury becomes irreversible. Such myocytes cannot be salvaged by reperfusion with arterial blood and are necrotic. When reperfused, irreversibly injured myocytes develop contraction-band necrosis and accumulate calcium phosphate. Although unproved, it is possible that some myocytes, alive at the time of reperfusion, may die as a consequence of successful reperfusion. This phenomenon is termed lethal reperfusion injury. Sublethal forms of reperfusion injury, such as stunning, also occur.

Acute Disease↗
PubMed1993

Reperfusion in acute myocardial infarction: effect of timing and modulating factors in experimental models.

Timely reperfusion of ischemic myocardium in experimental animals halts the advancing transmural "wavefront" of ischemic cell death and thereby limits myocardial infarct size by limiting its transmural extent. The time window of opportunity for such salvage in most experimental models of regional ischemia is the first 3 hours. The number of myocytes that can be salvaged by reperfusion decreases exponentially during this period, such that at 3 hours, reperfusion limits infarct size by only about 10%. The rate of lethal ischemic cell injury and therefore the amount of myocardium that can be salvaged by reperfusion after a particular duration of ischemia is dependent both on the degree of blood flow deficit and the rate of ischemic metabolism. In experimental animal models, several interventions, including hypothermia, calcium antagonists, and "ischemic preconditioning," have been shown to reduce the rate of ischemic metabolism and to limit myocardial infarct size when assessed after a defined period of ischemia and reperfusion. Hypothetically, interventions that could prevent additional myocyte necrosis caused by some deleterious aspects of reperfusion ("lethal reperfusion injury") also could serve as valuable adjunctive therapy. However, studies of therapies designed to prevent lethal reperfusion injury have produced conflicting results. Thus, the concept that lethal reperfusion injury occurs remains controversial. Experimental evidence indicates that reperfusion accelerates both the initial inflammatory response and later process of infarct repair. Late reperfusion of infarcts in dogs, which does not limit myocardial infarct size, appears to accelerate the replacement of necrotic myocardium by scar without altering the size of the final scar.

Animals↗
PubMed1993

Superoxide dismutase plus catalase therapy delays neither cell death nor the loss of the TTC reaction in experimental myocardial infarction in dogs.

Studies to test whether superoxide dismutase (SOD), with or without catalase, limits myocardial infarct size have produced conflicting results. Positive results following short periods of reperfusion vs negative results following longer periods of reperfusion could be explained if either: (1) myocytes, initially salvaged by SOD, are killed by continued production of free radicals after the administered SOD have been excreted, or (2) false positive results occur because SOD transiently preserves the TTC reaction, despite loss of cellular viability. To evaluate these two possibilities, we measured infarct size after 90 min of ischemia and 4 h of reperfusion in SOD+catalase treated and untreated dogs. Treated dogs received a 60 min intra-arterial infusion of SOD (15,000 U/kg) plus catalase (CAT) (55,000 U/kg) beginning 25 min before reperfusion. Infarct size was measured using triphenyl tetrazolium (TTC) macrochemistry and was compared with the extent of necrosis assessed semi-quantitatively by light microscopy. Mean infarct size was similar in the control and treated groups. In addition, there was a positive linear correlation (r = 0.95) between the extent of necrosis estimated by microscopy and that estimated by TTC in both groups, and treatment did not alter the regression line. These current results were compared with results from the control dogs from our previous study (Richard et al., 1988) in which 90 min of ischemia was followed by 4 days of reperfusion. TTC-based infarct size at 4 days of reperfusion was similar to that observed in both groups at 4 h. These data indicate that oxygen free radicals, accessible to intravascular SOD and catalase, are not a cause of myocyte death detectable by measurement of infarct size after 4 h of reperfusion. Moreover, neither an "early protection, delayed death" hypothesis nor a specific preservation of the TTC reaction explain the positive results of other studies. TTC macrochemistry provides reliable estimates of myocardial infarct size, provided that sufficient magnification is used to permit resolution of interdigitating peninsulas of viable and necrotic tissue.

Animals↗
PubMed1993

Cardiac protection by ischaemic preconditioning is not mediated by myocardial stunning.

OBJECTIVE: Previous studies have shown that cardiac protection by ischaemic preconditioning wanes before contractile function recovers; thus stunning is insufficient to cause preconditioning. To test whether reduced contractile effort is necessary for preconditioning induced protection, the effect on myocardial infarct size of restoring contractile function with dobutamine was examined in preconditioned and control dogs. METHODS: In two experimental groups (groups P and P+D), preconditioning was produced by four 5 min occlusions of the left anterior descending coronary artery, each separated by 5 min of reperfusion. Contractile function was assessed by sonomicrometry 5 min after completion of the preconditioning protocol. In group P+D, dobutamine (average dose = 5 micrograms.kg-1.min-1) was then infused intravenously to restore systolic shortening to baseline. The artery then was reoccluded for 40 min of sustained ischaemia followed by 4 d of reperfusion. Two additional groups of non-preconditioned control dogs (groups C and C+D) also underwent 40 min of coronary occlusion and 4 d of reperfusion. Group C+D received a dobutamine infusion beginning 15 min before and during the 40 min occlusion to match the dobutamine received in group P+D, whereas group C received normal saline. RESULTS: Preconditioning caused mild postischaemic contractile dysfunction (50% decrease in systolic shortening) which was easily reversed by dobutamine treatment. Dobutamine also increased both the rate-pressure product and the left ventricular dP/dt in both treated groups (C+D and P+D). Histological infarct size was 12.3(SEM 2.0)% of the area at risk in the untreated control group (n = 11), and was reduced to 4.4(1.7)% in the untreated preconditioning group (n = 8; p < 0.05). Dobutamine increased non-preconditioned infarct size (group C+D) to 22.1(3.4)% (n = 7; p < 0.05). Infarct size in the dobutamine treated preconditioning group (P+D) was not significantly different from infarct size in group P (n = 8), at 6.1(2.5%). CONCLUSIONS: In preconditioned hearts, dobutamine restored postischaemic contractile function but did not increase infarct size significantly. Thus reduced contractile effort is not required for the cardioprotective effect on ischaemic preconditioning.

Animals↗
PubMed1993

Adenosine slows ischaemic metabolism in canine myocardium in vitro: relationship to ischaemic preconditioning.

OBJECTIVE: Studies in rabbits suggest that the cardioprotective effects of adenosine against lethal cell injury may be related to production of adenosine and subsequent activation of adenosine A1 receptors. However, it is not known whether intracoronary adenosine therapy can mimic the metabolic sparing effects of preconditioning in rabbits or dogs. The purpose of this study was to determine the effect of intracoronary adenosine on ischaemic metabolism in totally ischaemic canine myocardium. METHODS: Dog hearts (n = 13) were excised and the coronary arteries were perfused with an oxygenated Krebs' buffer containing glucose. Adenosine was added to the buffer perfusing the circumflex (treated) region. Following perfusion, control and treated beds from each heart were subjected to 90 min total ischaemia at 37 degrees C. Tissue levels of ATP and glycolytic intermediates were determined at several time points during the ischaemic incubation. RESULTS: Adenosine significantly slowed the rate of ATP depletion, glycogen utilisation, and lactate accumulation during the first 20 minutes of total ischaemia. CONCLUSIONS: The results suggest that adenosine is capable of slowing ischaemic metabolism and they are consistent with the hypothesis that adenosine may mediate ischaemic preconditioning.

Adenosine↗
PubMed1993

Effect of anti-CD18 antibody on myocardial neutrophil accumulation and infarct size after ischemia and reperfusion in dogs.

BACKGROUND: Polymorphonuclear neutrophils (PMNs) accumulate in postischemic myocardium and may cause injury to myocardium or to vessels by production of oxygen free radicals or by release of proteases and lipases. PMN accumulation is dependent on adherence to endothelium, which is mediated by a family of glycoproteins on the PMN surface, each of which has a common beta-subunit (CD18). The purpose of this study was to determine whether an antibody (IB4) against the CD18 protein could attenuate PMN accumulation and limit myocardial infarct size. METHODS AND RESULTS: F(ab')2 fragments of a mouse monoclonal antibody to human adherence-promoting leukocyte glycoprotein (CD18) were used. Infarct size after 90 minutes of ischemia and 3 hours of reperfusion was compared in dogs with (n = 8) and without (n = 8) the anti-CD18 treatment. Myocardial PMN accumulation was assessed with 111In-labeled autologous PMNs. Anti-CD18 treatment significantly reduced the number of PMNs in the ischemic region (19,123 +/- 5,352/mg versus 5,204 +/- 927/mg in the control and treated groups, respectively; p < 0.05). In addition, the ratio of myocardial blood flow (ischemic/nonischemic wall) at 45 minutes into reperfusion was higher in the treated than in the control group (1.18 +/- 0.18 versus 0.69 +/- 0.09; p < 0.05). Nevertheless, infarct size was similar between the control and treated groups (40.5 +/- 7.4% versus 48.5 +/- 4.4% of the area at risk; p = NS). Transmural mean collateral blood flow to the ischemic myocardium was similar between the two groups, and the inverse relation between infarct size and collateral blood flow was not shifted by anti-CD18 therapy. CONCLUSIONS: Although PMN accumulation contributed to reduced postischemic microvascular perfusion, it caused insufficient additional myocardial cell death to measurably affect infarct size in this model.

Animals↗
PubMed1992

Correlation of the complete version of the Selvester QRS scoring system with quantitative anatomic findings for multiple left ventricular myocardial infarcts.

The correlation between myocardial infarct size estimated by the complete version of the Selvester QRS scoring system and that documented by pathoanatomic studies has been reported for single anterior, inferior and posterolateral infarcts. Although previous studies described electrocardiographic changes in patients with multiple infarcts, no quantitative documentation of the ability of such changes to estimate the total amount of left ventricular infarction has been reported. This study of 32 patients with anatomically documented multiple infarcts shows a significant correlation between QRS-estimated and anatomically documented sizes (r = 0.44; p = 0.01), which is less than that previously reported for single infarcts in the anterior, inferior and posterolateral locations. Several of the 54 electrocardiographic criteria were never satisfied. Criteria for posterior infarction were seldom present, suggesting "cancellation effect" of coexisting anterior infarction. These results will be the basis for future modification of QRS criteria for estimating myocardial infarct size.

Adult↗
PubMed1991

Preconditioning myocardium with ischemia.

Preconditioning and stunning are the chief adaptive changes induced in myocardium by a brief episode of reversible ischemia followed by arterial reperfusion. In the dog heart, both coexist for a period of at least 20 minutes of reperfusion, but after 120 minutes of reflow, preconditioning is much diminished, while stunning remains fully developed. Preconditioned, stunned, myocardium differs from control "virgin" myocardium in that adenine nucleotide content is reduced to about 50-70% of control, whereas creatine phosphate (CP) greatly exceeds normal--the so-called CP overshoot. When preconditioned myocardium is subjected to sustained ischemia, ATP utilization and anaerobic glycolysis occur at much slower rates than those observed in virgin myocardium. As a result of the early difference in metabolic rate, a longer period of ischemia is required for the ATP and lactate of the preconditioned tissue to reach the levels associated with irreversible injury. Associated with this change is a delay in myocyte death. The molecular events responsible for slower ischemic metabolism and associated tolerance of preconditioned, stunned tissue to a new ischemic episode are not known. Among the reactions that could cause a reduction in energy metabolism is reduced approximately P expenditure by stunned myocardium attempting to contract during the initial phase of ischemia. However, results from in vivo and in vitro experiments suggest that although stunning may be necessary for preconditioning to develop, it alone is not sufficient to cause preconditioning. Alternatively, metabolic changes may be explained by depressed activity of the mitochondrial ATPase during the episode of sustained ischemia. However, no direct experimental evidence supporting this hypothesis is available up to the present time.

Adenosine Triphosphate↗
PubMed1991

Effect of inhibition of the mitochondrial ATPase on net myocardial ATP in total ischemia.

The effect of inhibition of the mitochondrial ATPase with oligomycin on the rate of ATP depletion and anaerobic glycolysis was studied in the totally ischemic dog heart. An oxygenated, buffered crystalloidal solution containing 10 microM oligomycin and 12 mM glucose was delivered at 100 mmHg pressure to the circumflex bed of the excised cooled heart. Buffered solution without oligomycin was delivered simultaneously to the anterior descending bed of the same heart. Little metabolic evidence of ischemia developed until the heart was made totally ischemic by incubating it in a sealed plastic bag at 37 degrees C. Successful inhibition of the mitochondrial ATPase was confirmed by the absence of both mitochondrial ATPase activity and the loss of respiratory control in mitochondria isolated from treated tissue. ATP, glycolytic intermediates and catabolites of the adenine nucleotide pool were measured in the control and treated beds at various intervals during 120 min of ischemia. Inhibition of the ATPase resulted in slowing of the rates of ATP depletion and anaerobic glycolysis (estimated by lactate accumulation). Also, degradation of the adenine nucleotide pool occurred more slowly in the inhibited group. These data establish that about 35% of the ATP utilization observed during the first 90 min of total ischemia in the canine heart is due to mitochondrial ATPase activity.

Adenosine Triphosphatases↗
PubMed1991

Energy metabolism in preconditioned and control myocardium: effect of total ischemia.

Myocardium which has been preconditioned by one or several brief episodes of ischemia has much slower energy utilization during a subsequent sustained episode of ischemia. Since preconditioned tissue also is 'stunned', the reduced energy utilization of preconditioned tissue may be due to reduced contractile effort. This study was done to assess whether differences in energy utilization persisted or disappeared under conditions of total ischemia, in vitro, when contractile activity was abolished in both control and preconditioned regions by hyperkalemic cardiac arrest. Preconditioned myocardium was produced in open-chest anesthetized dogs by exposing the circumflex bed to four 5-min episodes of ischemia each followed by 5 min of arterial reperfusion. Non-preconditioned anterior descending bed was used as control myocardium. Hearts were arrested with hyperkalemia after the last reperfusion period in order to reduce or eliminate the effects of contractile activity. Metabolite content was measured in sequential biopsies of the tissue. Large differences in the rate of energy metabolism of the two regions were noted during the first 15 minutes of ischemia. During this time, the preconditioned tissue utilized less glycogen, and produced less lactate, glucose-6-phosphate (G6P), glucose-1-phosphate (G1P), and alpha-glycerol phosphate (alpha GP), than did control myocardium. Moreover, there was a much smaller decrease in net tissue ATP in the preconditioned than in the control tissue. Thus, the decrease in the demand of preconditioned tissue for energy, which has been observed in vivo, persisted despite the elimination of differences in contractile effort between control and preconditioned myocardium. Although the cause of this decrease in energy demand in preconditioned myocardium remains unknown, the present results suggest that it is not due to concomitant stunning.

Adenine Nucleotides↗
PubMed1991

Hypoxic reperfusion to remove ischaemic catabolites prior to arterial reperfusion does not limit the size of myocardial infarcts in dogs.

STUDY OBJECTIVE: Although timely reperfusion limits myocardial infarct size, it has been postulated that reperfusion itself may kill some myocytes which were alive at the end of an episode of ischaemia (lethal reperfusion injury). The aim of this study was to test the hypothesis that ischaemic catabolites may "prime" myocardium for such injury and that preliminary hypoxic washout of such catabolites, prior to arterial reperfusion, would limit myocardial infarct size. DESIGN: Dogs underwent a 40 min occlusion of the left circumflex coronary artery, followed by 4 d reperfusion. In a treated group, a 5 min episode of coronary artery perfusion with hypoxic buffer was instituted at the end of this ischaemic episode, before blood reperfusion was restored. Control dogs received a similar volume of hypoxic buffer intravenously. Systemic fluid overload was attenuated by haemofiltration. The effect of this preliminary hypoxic washout on myocardial infarct size was assessed. EXPERIMENTAL MATERIAL: 18 anaesthetised, open chest dogs were used. After the acute study they recovered from surgery for 4 d and were then killed for further study. MEASUREMENTS AND MAIN RESULTS: Infarct size, determined by microscopic evaluation, was not significantly different in the two groups, at (control) 31.3 (SEM 6.2)% v (hypoxic reperfusion) 25.8(3.9)% of the vascular area at risk. In control dogs, infarct size was inversely related to the amount of collateral blood flow (measured using microspheres); hypoxic reperfusion did not shift this relation (analysis of covariance, F = 0.236, NS). CONCLUSIONS: The washout of ischaemic catabolites by hypoxic perfusate prior to reoxygenation did not limit infarct size.

Animals↗
PubMed1991

The cell biology of acute myocardial ischemia.

The metabolic changes associated with the sudden onset of ischemia caused by occlusion of a major coronary artery include (a) cessation of aerobic metabolism, (b) depletion of creatine phosphate (CP), (c) onset of anaerobic glycolysis, and (d) accumulation of glycolytic products, such as lactate and alpha glycerol phosphate (alpha GP), and catabolites of the nucleotide pools in the tissue. These changes are associated with contractile failure and electrocardiographic alterations. Since the demand of the myocardium for high-energy phosphate (approximately P) exceeds the available supply, the net amount of ATP in tissue decreases. Eighty percent of the supply of approximately P utilized by severely ischemic tissue comes from anaerobic glycolysis using glycogen as the principal substrate. Early in ischemia, contractile activity utilizes ATP, but much of the continuing utilization of ATP by the ischemic tissue is energy wasted via the mitochondrial ATPase. A lesser quantity of ATP is used by ion transport ATPases. Metabolic changes slow as the duration of ischemia increases. Irreversibly injured myocytes exhibit (a) very low levels of ATP (less than 10% of control); (b) cessation of anaerobic glycolysis; (c) high levels of H+, AMP, INO, lactate, and alpha GP; (d) a greatly increased osmolar load; (e) mitochondrial swelling and formation of amorphous matrix densities; and (f) disruption of the sarcolemma. The latter event is generally recognized as lethal, but its pathogenesis remains to be established. Most severely ischemic myocytes are dead in regional ischemia in the anesthetized open-chest dog heart after only 60 minutes of ischemia. Less severely ischemic myocytes in the mid- and subepicardial myocardium survive for as long as six hours. Virtually all myocytes destined to die in a zone of ischemia are irreversibly injured after six hours of ischemia have passed. Certain changes exhibited by myocytes injured by severe ischemia and reperfused late in the reversible phase of injury do not return to the control conditions for a period of days, while others rebound in only seconds to minutes. The adenine nucleotide pool still is not fully restored after four days of reperfusion. Stunning disappears after one to two days of reflow. The preconditioning effect is partially lost after two hours of reperfusion. The timing of its disappearance has not been fully established. Aerobic metabolism is restored after only a few minutes of reperfusion. Thus, reperfusion salvages injured myocardium and restores its structure and function to the control state at a variable rate.

Animals↗
PubMed1991

Myocardial protection is lost before contractile function recovers from ischemic preconditioning.

Preconditioning myocardium with brief episodes of ischemia reduces energy demand and delays cell death during a subsequent ischemic episode. We hypothesized that postischemic contractile dysfunction after the brief ischemic episodes ("stunning") causes this reduced energy demand. If this hypothesis is correct, then cardioprotection should persist as long as mechanical function still is depressed at the onset of sustained ischemia. To analyze the temporal relationship between preconditioning and stunning, infarct size was compared in two groups of open-chest anesthetized dogs that were preconditioned with a 15-min coronary occlusion followed by a sustained 40-min occlusion. One group received 5 min of reperfusion and the second group received 120 min of reperfusion between occlusions. Nonpreconditioned controls received a single 40-min occlusion. A 15-min occlusion caused severe stunning, which did not improve during 2 h of reperfusion. In the 5-min reflow group, preconditioning resulted in dramatically smaller infarcts, averaging 2.2 +/- 0.9% of the area at risk vs. 26.5 +/- 4.2% in controls (P less than 0.01), confirmed by a marked shift in the inverse relationship between collateral blood flow and infarct size. Despite persistently severe stunning in the 120-min reflow group, infarct size was intermediate, averaging 12.3 +/- 2.7% (P less than 0.05 vs. 5-min reflow; P less than 0.01 vs. control), and the infarct vs. flow regression had returned toward control. Thus the cardioprotective effect of preconditioning was attenuated when the intervening reperfusion time was extended, even though severe contractile dysfunction persisted. We conclude that myocardial stunning, per se, is insufficient to cause preconditioning.

Animals↗
PubMed1991

Endocardial fibroelastosis with coronary artery thromboembolus and myocardial infarction.

We report a case of an 18-month-old male, born to a woman with third trimester febrile illness, who had a history of congestive heart failure and respiratory distress, cardiomegaly, and electrocardiographic (ECG) findings suggestive of cardiomyopathy and myocarditis. After gradual improvement in heart size and function with pharmacologic therapy, he developed a terminal episode of respiratory distress and cardiogenic shock, with ECG findings of an anterolateral infarct. At autopsy it was found that endocardial fibroelastosis with mural thrombi in the left ventricle had been complicated by thromboembolism to the left anterior descending coronary artery, resulting in transmural infarction of the anteroseptal region of the left ventricle. Myocardial infarction is a potential but unusual thromboembolic complication of endocardial fibroelastosis. A high index of suspicion for coronary artery thromboemboli should be maintained in pediatric patients with cardiomyopathy and suspected myocardial infarction.

Autopsy↗
PubMed1990

Sensitivity of a set of myocardial infarction screening criteria in patients with anatomically documented single and multiple infarcts.

A subset of 3 screening criteria (Q wave greater than or equal to 30 ms in lead aVF, any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV in lead V2, and R wave greater than or equal to 40 ms in V1) has been proposed to identify single nonacute myocardial infarcts. Cumulatively, these 3 criteria achieved 95% specificity, and 84 and 77% sensitivities for inferior and anterior myocardial infarcts, respectively, among patients identified by coronary angiography and left ventriculography. This study establishes the true sensitivities of the set of screening criteria in 71 patients with anatomically proven single myocardial infarcts and 32 patients with multiple myocardial infarcts. In the single inferior infarct group, the aVF criterion was 90% sensitive. The V2 criterion (any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV) was 67% sensitive in the single anterior infarct group. No single criterion proved sensitive in identifying a posterolateral infarct. The set of screening criteria performed just as well for multiple infarcts as it did for single infarcts, with a cumulative sensitivity of 72%. The overall sensitivity of the screening set in the 103 patients in all groups was 71%.

Adult↗
PubMed1990

Anatomic validation of electrocardiographic estimation of the size of acute or healed myocardial infarcts.

Seventeen new criteria added to the simplified version of the Selvester QRS scoring system to comprise the complete version were evaluated to determine their value in estimating the size of single infarcts. These non-Q-wave criteria might be particularly useful regarding posterolateral infarcts in the distribution of the left circumflex artery. The study population was made up of 21 anterior, 30 inferior and 20 posterolateral single myocardial infarction (MI) patients with no evidences of bundle branch or fascicular blocks, ventricular hypertrophy or previous MI on their final stable electrocardiogram. The complete system's maximum 32 points is capable of indicating MI in 96% of the left ventricle and it estimated a mean electrocardiographic MI size that better approximated the anatomic size compared with the simplified version in all MI locations. The correlation between anatomic and electrocardiographic MI size using the complete system was better and statistically significant for the posterolateral MI group (simplified r = 0.55, p less than 0.01 vs complete r = 0.70, p less than 0.0006). Criteria such as Q and S amplitude less than or equal to 0.3 mV in V1 and less than or equal to 0.4 mV in V2 were particularly helpful. This study documents the improved ability provided by the 17 additional non-Q-wave criteria which have been added in the complete version of this scoring system regarding the sizing of infarcts in the region of the left ventricle supplied by the left circumflex artery.

Electrocardiography↗