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We compared acute and late myocardial perfusion imaging using technetium-99m isotopes in 69 patients who had non-ST-elevation myocardial infarction. Among these patients, we found that the ischemic risk area was often large (19% of the left ventricle), and that 67% had significant myocardial salvage, defined as a >25% decrease in risk area, which was associated with an improved ejection fraction. [ABSTRACT FROM AUTHOR]

The prevalence of troponin elevations in patients with cardiac arrest (CA) using newer generation troponin assays when the ninety-ninth percentile is used has not been well described. We studied patients admitted with CA without ST elevation myocardial infarction (MI). Treatment included a multidisciplinary protocol that included routine use of hypothermia for appropriate patients. Serial assessment of cardiac biomarkers, including troponin I was obtained over the initial 24 to 36 hours. Patients were classified into 1 of 5 groups on the basis of multiples of the ninety-ninth percentile (upper reference limit [URL]), using the peak troponin I value: <1×, 1 to 3×, 3 to 5×, 5 to 10×, and >10×. Serial changes between the initial and second troponin I values were also assessed. A total of 165 patients with CA (mean age 58 ± 16, 67% men) were included. Troponin I was detectable in all but 2 patients (99%); all others had peak troponin I values that were greater than or equal to the URL. Most patients had peak troponin I values >10× URL, including patients with ventricular fibrillation or ventricular tachycardia (85%), asystole (50%), and pulseless electrical activity (59%). Serial changes in troponin I were present in almost all patients: ≥20% change in 162 (98%), ≥30% change in 159 (96%), and an absolute increase of ≥0.02 ng/ml in 85% of patients. In conclusion, almost all patients with CA who survived to admission had detectable troponin I, most of whom met biomarker guideline criteria for MI. Given the high mortality of these patients, these data have important implications for MI mortality reporting at CA treatment centers., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Few studies have examined associations between atherosclerotic risk factors and short-term mortality after first myocardial infarction (MI). Histories of 5 traditional atherosclerotic risk factors at presentation (diabetes, hypertension, smoking, dyslipidemia, and family history of premature heart disease) and hospital mortality were examined among 542,008 patients with first MIs in the National Registry of Myocardial Infarction (1994 to 2006). On initial MI presentation, history of hypertension (52.3%) was most common, followed by smoking (31.3%). The least common risk factor was diabetes (22.4%). Crude mortality was highest in patients with MI with diabetes (11.9%) and hypertension (9.8%) and lowest in those with smoking histories (5.4%) and dyslipidemia (4.6%). The inclusion of 5 atherosclerotic risk factors in a stepwise multivariate model contributed little toward predicting hospital mortality over age alone (C-statistic = 0.73 and 0.71, respectively). After extensive multivariate adjustments for clinical and sociodemographic factors, patients with MI with diabetes had higher odds of dying (odds ratio [OR] 1.23, 95% confidence interval [CI] 1.20 to 1.26) than those without diabetes and similarly for hypertension (OR 1.08, 95% CI 1.06 to 1.11). Conversely, family history (OR 0.71, 95% CI 0.69 to 0.73), dyslipidemia (OR 0.62, 95% CI 0.60 to 0.64), and smoking (OR 0.85, 95% CI 0.83 to 0.88) were associated with decreased mortality (C-statistic = 0.82 for the full model). In conclusion, in the setting of acute MI, histories of diabetes and hypertension are associated with higher hospital mortality, but the inclusion of atherosclerotic risk factors in models of hospital mortality does not improve predictive ability beyond other major clinical and sociodemographic characteristics., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Renal dysfunction is an important predictor of mortality in patients with acute coronary syndrome. Until recently, the Cockcroft-Gault (C-G) equation has been most commonly used to estimate renal function, although the Modification of Diet in Renal Disease (MDRD) equation is now recommended. Which equation better predicts mortality is unclear. Consecutive patients without ST elevation on the initial electrocardiogram admitted for exclusion of myocardial ischemia were included. Admission creatinine was used to estimate renal function, and 30-day and 1-year mortality were compared after classifying patients as having no (estimated glomerular filtration rate [eGFR] > or =60 ml/min/m(2)), moderate (eGFR 30 to 59 ml/min/ m(2)), or severe (eGFR <30 ml/min/m(2)) renal dysfunction using the 2 equations. Of the 4,343 patients (49% women, 64% African-American) included, 16% had troponin I elevations consistent with myocardial infarction, and 1-year mortality was 10%. Agreement between the 2 equations was high (r = 0.87 p <0.001, concordance 86%). Mortality was similar in the 2 renal function classifications, with no significant differences based on race or troponin I status at 30 days or 1 year. However, the area of the receiver operator characteristic curve was significantly larger for predicting 1-year mortality with the C-G equation (0.75 [0.72 to 0.77] vs 0.71 [0.68 to 0.73]; p <0.01); both were superior to creatinine alone (0.68 [0.66 to 0.71]; p <0.01 for both C-G and MDRD). Results for 30-day mortality were similar. In conclusion, the C-G equation appears to be superior to the MDRD equation for predicting short- and long-term mortality in patients admitted for exclusion of ischemia, although differences are minor.

Both the clinical and electrocardiographic presentations of sick sinus syndrome are highly variable. As illustrated by this month's case of Interactive Grand Rounds, the initial challenge to the clinician is to establish the correct diagnosis in the patient who has symptomatic bradyarrhythmias.

Most clinicians currently rely on patient history and specific electrocardiographic criteria to establish the diagnosis of arrhythmias. However, as illustrated by this case, the physical examination-especially auscultation of the first heart sound-can also provide useful diagnostic clues.

Early identification of acute myocardial infarction (AMI) is necessary to initiate appropriate treatment. In patients presenting without ST-segment elevation, diagnosis is often dependent on the presence of elevated myocardial markers. This study examines the ability of serial MB mass alone and in combination with myoglobin in diagnosing AMI in patients without ST-segment elevation within 3 hours of presentation. In all, 2,093 patients were admitted and underwent serial marker analysis using myoglobin, creatine kinase (CK), and CK-MB at 0, 3, 6, and 8 hours. AMI was diagnosed by a CK-MB > or =8.0 ng/ml and a relative index (RI) (CK-MB x 100/total CK) > or =4.0. A total of 186 patients (9%) were diagnosed with AMI. The optimal diagnostic strategy was an elevated CK-MB + RI on the initial or 3-hour sample or at least a twofold increase in CK-MB without exceeding the upper range of normal over the 3-hour time period (sensitivity 93%, specificity 98%). The combination of an elevated CK-MB + RI or myoglobin on the initial or 3-hour sample had a sensitivity of 94%, although specificity was significantly lower, at 86%. Sensitivities and specificities after exclusion of the 242 patients with ischemic electrocardiographic changes were essentially unchanged. We conclude that most patients with AMI presenting with nondiagnostic electrocardiograms can be diagnosed within 3 hours of presentation.

We analyzed the admission electrocardiogram in 109 patients with inferior wall acute myocardial infarction in an attempt to determine the infarct-related artery (IRA). The presence of ST depression in leads V1 or V2 had a high sensitivity for predicting the left circumflex artery as the IRA. The lack of ST depression in V1 or V2 had a high negative predictive value for excluding the left circumflex artery as the IRA.

This study further defines the mechanism of blood flow during closed-chest compression using transesophageal Doppler echocardiography. Although the echocardiographic demonstration of mitral valve closure during closed-chest compression has been used as evidence of direct cardiac compression, mitral valve closure has also been documented to occur during resuscitation by selectively increasing intrathoracic pressure. Transesophageal Doppler echocardiography was used to assess mitral valve position and flow in 17 adult patients undergoing cardiopulmonary resuscitation with a mechanical piston compression device. Left and right ventricular fractional shortening, mitral valve position with chest compression, timing and magnitude of transmitral flow, and anteroposterior chest diameter were recorded. In 12 patients (group I), the mitral valve closed during the down-stroke of chest compression; in the remaining 5 (group II), it opened further. Peak transmitral flow occurred during the release phase and was significantly higher (p < 0.05) in group I (39.5 +/- 9.3 cm/s) than the peak flow in group II (21.3 +/- 5.9 cm/s), which occurred during the downstroke of chest compression. Left ventricular fractional shortening inversely correlated (r = -0.68; p = 0.02) with the anteroposterior chest diameter, but did not correlate with peak transmitral flow (r = 0.34; p = not significant). It is concluded that the mitral valve closes during the downstroke of chest compression in most adult patients during resuscitation. The absence of a relation between mitral valve flow and left ventricular fractional shortening supports the hypothesis that other factors such as nonuniform increases in intrathoracic pressure cause the mitral valve to open or close during chest compression.