Extent Of Acute Myocardial Infarction Research Articles

Association of HBA1C level with extent of Acute Myocardial Infarction and Short Term Mortality

ABSTRACT Objectives: To determine the prognostic value of HBA1C level with extent of acute Myocardial Infarction (MI) and short-term mortality in patients without known Diabetes. MATERIAL AND METHODS The prospective cohort, department of Cardiology at Liaquat University Hospital Hyderabad during the period of one year from February 2020 January 2021. All the patients aged 20-75 years, both genders with acute MI (STEMI and NSTEMI) were included. All the patients diagnosed for MI according to ECG and serum cardiac biomarkers such as Troponin-T and Troponin-I. Blood sample were taken from all the cases for assessment of HbA1c level. Echocardiography was done and categorized according to the left ventricle ejection fraction. Short term mortality was assessed in all patients. All the data was recorded in the proforma for the purpose of analysis. After collection of data the analysis was conducted by using SPSS version 22.0. Results: Total 377 patients of acute MI were studied; their mean age was 50.42+11.71 years. Out of all study subjects’ males were in majority 83.0% and females were 17.0%. Out of all 59.4% had HbA1c level <5.5 and 40.6% had HbA1c was <6.5. Most of the study subjects 62.9% had left ventricular ejection fraction was <40%. Majority of the cases 77.7% had STEMI and NSTEMI was seen in 22.3% of the cases. Overall short-term mortality (30 days) was found 14.3%. In this study short term mortality (30 days) was statistically significant according to the gender, HbA1c, left ventricular ejection fraction and types of the MI, P-<0.05). Conclusion: As pers study conclusion overall short-term mortality (30 days) was 14.3%. Higher HbA1c was observed to be a potential indicator for short term mortality among patients of acute coronary syndrome (ACS) and a predictor for short-term mortality in ACS patients without known DM and without DM Key words: Acute MI, 30 days mortality, Hba1c

Dysbiotic microbiota contributes to the extent of acute myocardial infarction in rats

Increasing evidence suggests that the intestinal microbiota composition could play a role in specific pathologies such as hypertension, obesity and diabetes. This study aims to demonstrate that the intestinal microbiota modulated by a diet creating dysbiosis increased the size of the myocardial infarction and that probiotics could attenuate this effect. To do this, microbiota transplants from rats fed a dysbiotic or non-dysbiotic diet in the presence or absence of probiotics were performed for 10 days on rats whose microbiota had been previously suppressed by antibiotic therapy. Then, the anterior coronary artery of the transplanted rats was occluded for 30 min. Infarct size was measured after 24 h of reperfusion, while signaling pathways were evaluated after 15 min of reperfusion. Intestinal resistance, plasma concentration of LPS (lipopolysaccharides), activation of NF-κB and Akt and composition of the microbiota were also measured. Our results demonstrate a larger infarct size in animals transplanted with the dysbiotic microbiota without probiotics compared to the other groups, including those that received the dysbiotic microbiota with probiotics. This increase in infarct size correlates with a higher firmicutes/bacteroidetes ratio, NF-kB phosphorylation and plasma LPS concentration, and a decrease in intestinal barrier resistance and Akt. These results indicate that dysbiotic microbiota promotes an increase in infarct size, an effect that probiotics can attenuate.

Letter by Madias Regarding Article, “Peripheral Nociception Associated With Surgical Incision Elicits Remote Nonischemic Cardioprotection via Neurogenic Activation of Protein Kinase C Signaling”

HomeCirculationVol. 121, No. 16Letter by Madias Regarding Article, “Peripheral Nociception Associated With Surgical Incision Elicits Remote Nonischemic Cardioprotection via Neurogenic Activation of Protein Kinase C Signaling” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Madias Regarding Article, “Peripheral Nociception Associated With Surgical Incision Elicits Remote Nonischemic Cardioprotection via Neurogenic Activation of Protein Kinase C Signaling” John E. Madias, MD John E. MadiasJohn E. Madias Mount Sinai School of Medicine, New York University, New York, NY Search for more papers by this author Originally published27 Apr 2010https://doi.org/10.1161/CIR.0b013e3181ddf949Circulation. 2010;121:e388To the Editor:The elegant study of Jones et al1 on peripheral nociception-based remote nonischemic preconditioning, published in the September 15, 2009, issue of Circulation, constitutes an advancement in the field of noninvasive cardioprotection for ischemic/reperfusion injury. Not only were the authors able to establish that peripheral skin nociception, resulting from abdominal surgical incision in their murine model and via the axis of neurogenic signaling–bradykinin stimulation of bradykinin 2 receptors–KATP channels, leads to marked reduction in eventual infarct size, but by implementing topical capsaicin in parallel experiments, they also showed that its selective stimulation of skin C sensory fibers leads to equally marked cardioprotection, as could be ascertained from a comparison of Figures 2 and 7 in their article. The authors emphasize that this novel cardioprotective phenomenon is associated with an 80% decrease in infarct size, the largest such beneficial effect described in a murine model. They stress that capsaicin is already approved by the Food and Drug Administration, is used to treat pain, and is devoid of serious adverse effects. Thus, if shown to be effective in humans, this simple therapy has the potential to reduce myocardial injury in the setting of ischemia/reperfusion, thereby reducing the extent and consequences of acute myocardial infarction. However, in reviewing the parallel experiments that these authors have carried out, one cannot overlook that the intervention (either abdominal incision or topical capsaicin application) was implemented before the inception of the 45 minutes of myocardial ischemia and the subsequent reperfusion. Thus, this study design allows the “therapeutic” interventions to qualify as nociception-based remote nonischemic preconditioning, whereas the clinical reality permits only “ischemic and nonischemic postconditioning” implementation for patients who have experienced an acute myocardial infarction. Perhaps the authors could supplement their observations by performing a study in which topical application of capsaicin is implemented after the inception of the 45-minute period of ischemia and during reperfusion; such additional experiments will provide clinical insight into what effects “capsaicin nonischemic postconditioning” could be expected to have in patients with an acute myocardial infarction already in progress before and after reperfusion therapy, by either primary percutaneous coronary intervention or thrombolysis. Whether postconditioning is beneficial in the setting of acute myocardial infarction is still controversial on the basis of animal studies in which very brief periods of coronary ischemic postconditioning in the early phase of reperfusion did not alter the extent of acute myocardial infarction in the rabbit,2 whereas remote postconditioning did reduce the infarct size in the pig.3 The authors could help by contributing in this pivotal area.DisclosuresNone. References 1 Jones WK, Fan GC, Liao S, Zhang JM, Wang Y, Weintraub NL, Kranias EG, Schultz JE, Lorenz J, Ren X. Peripheral nociception associated with surgical incision elicits remote nonischemic cardioprotection via neurogenic activation of protein kinase C signaling. Circulation. 2009; 120 (suppl): S1–S9.LinkGoogle Scholar2 Hale SL, Mehra A, Leeka J, Kloner RA. Postconditioning fails to improve no reflow or alter infarct size in an open-chest rabbit model of myocardial ischemia-reperfusion. Am J Physiol Heart Circ Physiol. 2008; 294: H421–H425.CrossrefMedlineGoogle Scholar3 Andreka G, Vertesaljai M, Szantho G, Font G, Piroth Z, Fontos G, Juhasz ED, Szekely L, Szelid Z, Turner MS, Ashrafian H, Frenneaux MP, Andreka P. Remote ischaemic postconditioning protects the heart during acute myocardial infarction in pigs. Heart. 2007; 93: 749–752.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails April 27, 2010Vol 121, Issue 16 Advertisement Article InformationMetrics https://doi.org/10.1161/CIR.0b013e3181ddf949PMID: 20421525 Originally publishedApril 27, 2010 PDF download Advertisement SubjectsAcute Coronary SyndromesMyocardial Infarction

Relation Between Signal Intensity on T2-Weighted MR Images and Presence of Microvascular Obstruction in Patients With Acute Myocardial Infarction

In experimental animal models and human autopsy studies, hemorrhagic infarction caused by microvascular injury has been detected after coronary reperfusion. The purpose of this study was to determine whether detection of myocardial edema with T2-weighted MRI is influenced by the presence of microvascular obstruction. Thirty-seven patients underwent black-blood fat-suppressed T2-weighted, rest perfusion, and late gadolinium-enhanced MRI 5.4 +/- 3.1 days after the onset of acute myocardial infarction. On T2-weighted MR images, the signal intensity in relation to that of remote myocardium was determined in the late gadolinium-enhanced and periinfarction areas. Segment-based analysis was performed to determine whether the presence of microvascular obstruction influences the detection of myocardial edema. The averaged signal intensity in the late gadolinium-enhanced area without microvascular obstruction was significantly higher than the signal intensity in remote normal myocardium (relative signal intensity, 1.83 +/- 0.50; p < 0.001). In contrast, the signal intensity in the microvascular obstruction area on T2-weighted images was not significantly different from the signal intensity in remote myocardium (relative signal intensity, 1.14 +/- 0.26). The percentages of late gadolinium-enhanced segments with high signal intensity on T2-weighted MR images were 95% (73/77) without microvascular obstruction and 30% (22/73) with microvascular obstruction. With T2-weighted MRI, infarction-associated edema can be reliably detected in infarct lesions without microvascular obstruction. Microvascular obstruction, however, does not necessarily exhibit high signal intensity on T2-weighted MRI. Careful attention is required in interpretation of cardiac MR images of patients who have experienced acute myocardial infarction and undergone percutaneous coronary intervention. The findings on T2-weighted MR images can be substantial underestimates of the extent of acute myocardial infarction.

222 Cardiac magnetic resonance assessment of induced myocardial infarction and reverse remodelling early after alcohol septal ablation

Objectives and background Magnetic resonance imaging (MRI) has been used to delineate the extent of acute myocardial infarction in coronary artery disease, but its role after ethanol induced septal infarction has not been largely assessed. We report the evaluation of septal infarction induced by alcohol septal ablation (ASA) in patients with symptomatic hypertrophic obstructive cardiomyopathy using contrast enhanced MRI.

1036 Semi-quantitative segmental scores is an accurate method in determing the size and extent of acute myocardial infarction

1036 Semi-quantitative segmental scores is an accurate method in determing the size and extent of acute myocardial infarction

Assessment of Acute Myocardial Infarction Using MDCT After Percutaneous Coronary Intervention: Comparison with MRI

Imaging to determine myocardial infarct size is difficult in the emergency setting because the current gold standards, MRI and nuclear medicine techniques, are difficult to perform in unstable patients. Delayed enhanced MDCT has recently been proposed as a technique to study contrast uptake in infarcted myocardium. In this study, we compared the extent of acute myocardial infarction as measured by delayed enhanced MDCT performed immediately after percutaneous coronary intervention (PCI) without an additional iodine injection with that measured by delayed gadolinium-enhanced MRI. Nineteen consecutive patients presenting with primary acute myocardial infarction underwent delayed enhanced MDCT immediately after coronary angioplasty and underwent delayed enhanced MRI within 8 days of angioplasty. Only patients with a thrombolysis in myocardial infarction (TIMI) score of 0 or 1 of the culprit coronary artery before endovascular angioplasty and TIMI score of 2 or 3 after angioplasty were selected. Comparison of delayed enhanced MDCT and delayed enhanced MRI was performed by three observers and focused on identifying the involved segments and determining the transmural extent of enhancement and infarct size. The mean signal intensity was significantly higher in the involved territory than in healthy myocardium: 197 +/- 81 H versus 71 +/- 20 H, respectively (p < 0.0001). We found significant agreement between delayed enhanced MDCT and delayed enhanced MRI for the number of involved segments, transmural extent of enhancement, and infarct size (r(2) = 0.74, 0.76, and 0.67, respectively; p < 0.0001) with good interobserver reproducibility (kappa = 0.8). The results of our study show that delayed enhanced MDCT allows accurate visualization of early myocardial contrast uptake compared with delayed enhanced MRI and does not require an additional contrast injection after PCI.

Determination of Size and Transmural Extent of Acute Myocardial Infarction by Real-time Myocardial Perfusion Echocardiography: A Comparison with Magnetic Resonance Imaging

The exact determination of acute myocardial infarction (AMI) extent is still a challenging issue. Quantitative myocardial perfusion echocardiography (MPE) with parametric imaging (PI) and gray scale (GS) has been shown to accurately measure infarcted area in animals, but not in human beings. We sought to validate MPE quantification of transmural extent and size of AMI using magnetic resonance imaging (MRI) as a gold standard. Twenty patients (12 men, 64 +/- 13 years) underwent MPE and MRI between the second and fifth day post-AMI. Infarct area and location, number of involved segments, and transmural extent in each segment were determined by PI using beta value and GS. Results were compared with late enhanced MRI. There was 99% agreement between both methods regarding the segmental location. The correlation between infarct area by MRI and GS was 0.82 (P < .001) whereas MRI and beta PI was 0.92 (P < .001). The correlation between transmural extent by MRI and GS was 0.77 (P < .001), and between MRI and beta PI was 0.93 (P < .001). There was a good correlation between MPE, in special beta PI, with MRI in measuring infarcted area and its transmural extent in patients with AMI.

Size and transmural extent of first-time reperfused myocardial infarction assessed by cardiac magnetic resonance can be estimated by 12-lead electrocardiogram

The ability of the 12-lead electrocardiogram (ECG) to quantify size and transmural extent of myocardial infarction (MI) is not fully explored. Q waves are still thought of as indicative of transmural MI despite that several studies have rejected this association. We hypothesized that size and transmural extent of acute MI indeed can be estimated by QRS scoring on the 12-lead ECG using delayed, contrast-enhanced magnetic resonance imaging (DE-MRI) as gold standard and that Q waves are not predictive of transmural MI. Twenty-nine patients with first-time reperfused MI were studied. Delayed, contrast-enhanced magnetic resonance imaging was performed and 12-lead ECG was recorded 8 +/- 1 days after the acute event. Myocardial infarction size and transmurality were determined by DE-MRI and compared with Selvester QRS score from the ECG recorded on the same day. There was a good correlation (r = 0.79, P < .001) between MI size by QRS scoring and DE-MRI. As local MI transmurality increased as assessed by DE-MRI, the local QRS score increased progressively (P < .001). There was no significant difference in the number of Q-wave-related QRS points between nontransmural and transmural MI (1.8 +/- 0.6 vs 2.9 +/- 0.4, P = .14). The global QRS score, however, differed significantly (3.1 +/- 0.8 vs 5.1 +/- 0.6, P < .05). QRS score is significantly related to both MI size and transmurality by DE-MRI in patients with first-time reperfused MI. Presence of Q waves, however, is not indicative of transmural MI in these patients. Thus, QRS scoring could potentially be used for diagnosing and characterizing MI in patients with suspected recent MI.

Antioxidant vitamin levels do not exhibit negative correlation with the extent of acute myocardial infarction.

Serum levels of vitamin E (VE), beta-carotene (BC) and vitamin C (VC) were determined in 50 patients with the first acute myocardial infarction (AMI) before starting thrombolytical treatment. VE and BC were determined by HPLC, VC spectrophotometrically. The reperfused patients were divided according to vitamin concentrations into four groups. The lowest quartile was compared with the rest of the studied population (VE: group with high (H)>15.6 microM>group with low (L), BC: H>0.07 microM>L, VC: H>25 microM>L) in the following parameters: extent of myocardial damage (area under the curves of troponin I, CK-MB during 48 h), arrhythmia and congestive heart failure occurrence, size of ejection fraction, positivity of ventricular late potentials. No significant differences between groups H and L for either VE, BC or VC were found (P 0.05). As no correlation between serum concentrations of vitamins E, C and beta-carotene and the extent and clinical course of AMI was found, the actual vitamin concentrations may be important for prevention of ischemic heart a disease, but they do not play a decisive role in the acute phase of myocardial infarction in humans.

Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function

Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function

Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function.

Previous animal studies have demonstrated that the transmural extent of acute myocardial infarction defined by contrast-enhanced MRI (ceMRI) relates to early restoration of flow and future improvements in contractile function. We tested the hypothesis that ceMRI would have similar predictive value in humans. Twenty-four patients who presented with their first myocardial infarction and were successfully revascularized underwent cine and ceMRI of their heart within 7 days (scan 1) of the peak MB band of creatine kinase. Cine MRI was repeated 8 to 12 weeks later (scan 2). The transmural extent of infarction on scan 1 and wall thickening on both scans were determined using a 72-segment model. A total of 524 of 1571 segments (33%) were dysfunctional on scan 1. Improvement in segmental contractile function on scan 2 was inversely related to the transmural extent of infarction on scan 1 (P=0.001). Improvement in global contractile function, as assessed by ejection fraction and mean wall thickening score, was not predicted by peak creatine kinase-MB (P=0.66) or by total infarct size, as defined by MRI (P=0.70). The best predictor of global improvement was the extent of dysfunctional myocardium that was not infarcted or had infarction comprising <25% of left ventricular wall thickness (P<0.005 for ejection fraction, P<0.001 for mean wall thickening score). In patients with acute myocardial infarction, the transmural extent of infarction defined by ceMRI predicts improvement in contractile function.

35. Haemostatic factors in the prediction of the extent of acute myocardial infarction

35. Haemostatic factors in the prediction of the extent of acute myocardial infarction

Intravenous atenolol in elderly patients in the early phase of acute myocardial infarction.

The aim of this study was to assess the hemodynamic response to intravenous atenolol in elderly patients with acute myocardial infarction. We studied 14 elderly men, aged 64-85 years, and 14 younger men, aged 29-48 years, in the early postfibrinolytic phase of acute myocardial infarction. All the patients were in Killip class I. A triple-lumen Swan-Ganz thermodilution catheter was introduced into the right heart chambers. The patients received 5 mg intravenous atenolol over 5 minutes. All hemodynamic parameters were measured before and 10 minutes after atenolol. The hemodynamic characteristics and the location and extent of acute myocardial infarction were the same in both groups before atenolol. The hemodynamic changes after atenolol administration were the same in the two groups, but the stroke volume and cardiac indexes decreased to a greater extent in the elderly (p = .01 and p = .0001, respectively). These results indicate that intravenous atenolol in the early postfibrinolytic phase of acute myocardial infarction is safe in Killip class I elderly patients, although the cardiac and stroke volume indexes decrease, and the increase in the total systemic resistance is more in older than in younger patients.

Quantitation of the extent of acute myocardial infarction by phosphorus-31 nuclear magnetic resonance spectroscopy

Phosphorus-31 nuclear magnetic resonance (P-31 NMR) spectroscopy is able to identify alterations in myocardial high energy phosphate metabolism associated with acute infarction. It was hypothesized that the extent of acute myocardial infarction could be quantitated from changes in the tissue content of inorganic phosphate (P1), phosphocreatine (PCr) and adenosine triphosphate (ATP) derived from P-31 NMR spectra.Nine isolated, perfused rat hearts were studied at 121.5 MHz. After baseline spectra were obtained, varying locations of either the right or the left coronary artery were occluded without removing the heart from the spectrometer. Spectra were then collected during regional ischemia at 15 and 45 min after occlusion. Phosphate metabolites were quantitated from the baseline and 45-min regional ischemia spectra, times at which the metabolites are at steady state for the normal and ischemic conditions. The heart was removed from the spectrometer, perfused for a total duration of 2 h and sectioned into 2-mm thick slices for triphenyltetrazolium chloride staining. Percent infarct was determined by manual tracing of magnified, digitized images of the stained sections. Coronary blood flow, heart rate and blood pressure were monitored throughout the experiment.Significant linear relations were found between percent infarct (by triphenyltetrazolium chloride staining) and the percent change of beta-ATP (r = −0.74), Pi(r = 0.83) and the PCr/P1 ratio (r = −0.71) at 45 min after coronary occlusion. Coronary Row was also found to correlate significantly with percent infarct (r = −0.70).These results are applicable to in vivo P-31 NMR studies of acute infarction where the volume of interest may include both normal and acutely infarcled myocardium. It is concluded that changes in P-31 NMR spectra allow quantitation of the extent of acute myocardial infarction.

Quantitation of the extent of acute myocardial infarction by phosphorus-31 nuclear magnetic resonance spectroscopy

Quantitation of the extent of acute myocardial infarction by phosphorus-31 nuclear magnetic resonance spectroscopy

Relation between the transmural extent of acute myocardial infarction and associated myocardial contractility two weeks after infarction

To characterize the relation between the transmural extent of acute myocardial infarction (AMI) and associated regional contractility after recovery from ischemia, 11 mongrel dogs underwent occlusion of the proximal left anterior descending coronary artery and were evaluated 2 weeks after infarction. Occlusion was permanent in 5 dogs, and reperfusion was allowed after 2 hours of occlusion in 6 dogs. All dogs had computer-assisted quantitative wallthickening analysis by 2-dimensional echocardiography and infarct localization by the triphenyltetrazolium chloride technique. Percent systolic wall thickening was correlated with the transmural extent of AMI in 40 regions of interest, each measuring aproximately 60 arc degrees in circumference. In 11 non-infarct-containing regions, the mean wall thickening was 59 ± 16% (± standard deviation). In 29 infarct-containing segments (with transmural extent of infarction 11 to 100%) systolic wall thickening ranged from −4% to 47%. Wall thickening and transmural extent of AMI were inversely related. Least-squares regression analysis found the relation to be best described by the logarithmic function, percent wall thickening = 61 − 26 log (percent transmural extent of infarction +1), r = −0.87. The nature of this relation between structure and function suggests that salvage of small amounts of myocardium (transmural extent less than 30 to 40%) by coronary reperfusion or other means may have little effect on systolic myocardial function when compared with the function of transmural infarcts. Alternatively, salvage of more than 40 % of the jeopardized myocardium should be expected to appreciably augment myocardial function.

Thallium-201 versus technetium-99m pyrophosphate myocardial imaging in detection and evaluation of patients with acute myocardial infarction

Thallium-201 myocardial imaging is of value in the early detection and evaluation of patients with suspected acute infarction. The extent of a thallium defect in an initial myocardial image may have important prognostic value. Tomographic imaging techniques hold promise for increased diagnostic sensitivity and more accurate quantitation of both infarcted and residual viable myocardium. Thallium imaging may have a special value in characterizing patients with cardiogenic shock and in detecting patients at risk for subsequent infarction or death or both, before hospital discharge. Approximately 95 percent of patients with transmural or nontransmural myocardial infarction can be detected with technetium-99m pyrophos-phate myocardial imaging if the imaging is performed 24 to 72 hours after the onset of symptoms. Pyrophosphate imaging has been useful in localizing the site and determining the extent of acute myocardial infarction. The “doughnut” pattern is associated with a relatively large incidence of subsequent congestive heart failure and death. However, the clinical utility of this information is limited because it is usually not available when it is most needed, on admission to the coronary care unit. Pyrophosphate imaging may have an important role in the evaluation of patients during the early follow-up period after hospital discharge from an episode of acute infarction. The finding of a persistently positive pyrophosphate image suggests a poor prognosis and is associated with a relatively large incidence of subsequent myocardial infarction and death.

Echoventriculography in acute myocardial infarction. IV. Infarct size and reliability by pathologic anatomic correlations.

A morphologic-echocardiographic comparison was carried out in 24 consecutive patients to determine the accuracy of multidirectional single-beam echocardiography in imaging the size and site of 22 fatal acute myocardial infarctions and of 2 postinfarction ventricular aneurysms treated surgically. Echocardiography never missed the infarction, regardless of whether the infarction was anterior or posterior. The correlation between the echocardiographic and pathologic anatomic extent of infarct, as expressed by a percentage of the left ventricular horizontal circumference, was r=0.88 (p less than 0.001). One hundred four of one hundred eleven infarcted segments (94%) were detected by echo; only the posterior septal and the most lateral segments of the left ventricle tended to remain out of range of the method. The regional asynergy at the center of the infarcted region was clearcut-systolic thickening was never seen and the systolic wall motion was paradoxical in 75% of the patients (mean, -20+/-2.0 mm). Analysis of the regional function from multiple sites characterized reduction of the left ventricular performance (p less than 0.0005) better than did the ejection fraction in the presence of asynergy. An old postinfarction scar was differentiated from the acute necrosis. Thus, segmental left ventricular akinesis or paradoxical motion as seen by multidirectional echocardiography permits noninvasively a reliable estimation of the extent of acute myocardial infarction.

Myocardial imaging with radioactive potassium and its analogs

G OALS common to both the clinical and investigative study of coronary heart disease concern accurate detection and definition of the site and extent of acute myocardial infarction, myocardial scar, and reversible myocardial ischemia. Radionuclide myocardial imaging techniques offer the possibility of ultimately fulfilling at least a portion of these goals. The increasing prevalence of the various myocardial imaging approaches over the past 5 yr has been due in part to major advances in instrumentation, development of new radiopharmaceuticals, and application of computer technology to standard clinical nuclear imaging. Early recognition of the association between acute myocardial ischemia and infarction and abnormality in regional potassium metabolism led to investigation of the possibility of utilizing radioactive potassium or radioactive potassium analogs to define abnormalities in the diseased atherosclerotic heart. When these radioactive cations are administered intravenously, sufficient myocardial uptake occurs to allow external detection or imaging of a myocardial radioactivity distribution. This distribution displays zones of infarction or ischemia as “cold spots,” or regions of relatively decreased to