The role of biochemical markers in the diagnosis of acute coronary syndromes has increased considerably in the past decade. The World Health Organization previously defined acute myocardial infarction as a combination of at least 2 of 3 components: symptoms consistent with acute myocardial infarction, electrocardiogram changes diagnostic of acute myocardial infarction, and an enzyme pattern with classic rise and fall. Measurement of creatine kinase and its MB fraction by various assays was the gold standard for the diagnosis. Troponins are more specific and sensitive markers for myocardial injury, and their increasing utilization has resulted in a broadening of the definition of acute myocardial infarction to incorporate high-risk acute coronary syndromes. Previously, traditional enzyme evaluation left patients with small amounts of cellular death undiagnosed; these patients were categorized as having unstable angina or, worse, noncardiac chest pain. Newer markers now identify these patients as a subgroup at high risk for cardiac death or cardiac events. Newer therapeutic interventions and a more invasive strategy have been shown to improve outcomes in this high-risk subgroup. Increased specificity has also reduced the number of patients who undergo extensive, expensive, and invasive evaluations for noncardiac syndromes due to false elevations of traditional markers. This article comprehensively reviews the evolution of biochemical markers for the diagnosis of acute myocardial infarction, addressing their promise for improving delivery of care and outcomes and their technical and diagnostic pitfalls.

Background: Rates of cardiovascular disease and its risk factors seem to be increasing in American Indian populations, yet these changes have received little documentation.

A 69-year-old female was admitted with the diagnosis of a non-ST-segment elevation myocardial infarction and placed on cardiac telemetry. Her resting ECG showed sinus rhythm and voltage criteria for left ventricular hypertrophy. A tracing was recorded by the telemetry monitor (Philips Med Systems) ( Figure 1); the patient was asymptomatic. What is the mechanism for the sudden change in QRS morphology?The telemetry tracing shows lead II (top, channel 1) and midclavicular line (MCL) (bottom, channel 2). The rhythm is a regular sinus tachycardia at 120 bpm. There is no significant lead noise or other apparent recording artefact. The QRS morphology changes abruptly (10th QRS) without any change in heart rate or rhythm. This suggested a nonphysiological cause for the change in QRS morphology. Upon closer inspection it becomes apparent that the change in QRS morphology appears to be due to a switch between the recording leads. This is indeed normal behaviour for this multi-lead Philips telemetry monitoring system and is referred to as 'fall back' operation mode.The user manual explains: 'If there is a lead OFF in the primary lead (channel 1) for .10 s, the active secondary lead (channel 2) becomes the primary lead. This is known as 'lead fallback'. In the lead fallback, the arrhythmia system switches the leads on the display. When the lead OFF condition is corrected, the leads are switched back'.Indeed 12 s prior to the change in QRS morphology (10th QRS), both recording leads were off (not shown). Upon reconnect the 'lead fallback' algorithm had already triggered a 'lead switch' and upon recognizing both leads as reconnected the system switched the leads back to its original display (last seven QRS complexes on telemetry strip). This is followed by relearning of the rhythm as indicated by the letter N next to the QRS complexes. There is no annotation on the display or printout alerting the observer to the 'fall back' mode operation.Our case illustrates that appropriate, yet not immediately obvious, arrhythmia monitoring system behaviour can result in a potential diagnostic dilemma.& The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Results:Patients with liver disease were younger and represented more minorities in comparison to patients without liver disease undergoing PCI. They had significantly higher rates of renal and pulmonary disease and were more likely to be on insulin therapy, but had a similar prevalence of prior coronary artery disease history, myocardial infarction, heart failure and cardiac risk factors. Rates of multivessel disease, intervention success and anti-platelet therapy were not significantly different between groups. There was no increased incidence of peri-procedural complications including bleeding requiring transfusion (pϭ0.29), major entry site complications (pϭ0.70), and stroke (pϭ0.70). At 1 year, cumulative event rates, including death, myocardial infarction, coronary artery bypass graft surgery, and repeat PCI were similar between the groups (Table 1).Background: Cardiovascular (CV) disease is the leading cause of mortality among women in the US. Despite targeted public health initiatives, many women remain unaware of and undertreated for their CV risk factors. Methods: We surveyed women presenting to obstetrics and gynecology (OB/GYN) clinics for the presence of traditional and non-traditional CV risk factors and any current symptoms using a simple, one-page questionnaire. Blood pressure and cholesterol were measured if there was no prior screening. Results: 2,863 patients were surveyed at 16 US centers from May 2010 to June 2012. The mean age was 51 Ϯ 14 years. 45% were post-menopausal. The majority of pts had no prior diagnosis of myocardial infarction, angina or stroke (96%). However, 82% of women had at least one CV risk factor (figure) and 41% had a CV complaint such as chest pain, dyspnea, or palpitations. A significant proportion of women did not know if they had diabetes, hyperlipidemia or hypertension (18%, 36% and 18% respectively). 74% of women had a primary care physician (PCP). As a result of screening, 25% of patients were referred to another health care provider, in most of cases to a PCP (45%) or a cardiologist (28%). Conclusions: Screening women presenting to community OB/GYN clinics with a one-page questionnaire in this pilot, multicenter program, revealed a high prevalence of CV risk factors and symptoms, and may enhance the early detection and treatment of CV disease in female patients. Whether screening patients in this setting will translate into improved long-term outcomes warrants further evaluation.

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