Type 2 myocardial infarction: the chimaera of cardiology?

The term type 2 myocardial infarction first appeared as part of the universal definition of myocardial infarction. It was introduced to cover a group of patients who had elevation of cardiac troponin but did not meet the traditional criteria for acute myocardial infarction although they were considered to have an underlying ischaemic aetiology for the myocardial damage observed. Since first inception, the term type 2 myocardial infarction has always been vague. Although attempts have been made to produce a systematic definition of what constitutes a type 2 myocardial infarction, it has been more often characterised by what it is not rather than what it is. Clinical studies that have used type 2 myocardial infarction as a diagnostic criterion have produced disparate incidence figures. The range of associated clinical conditions differs from study to study. Additionally, there are no agreed or evidence-based treatment strategies for type 2 myocardial infarction. The authors believe that the term type 2 myocardial infarction is confusing and not evidence-based. They consider that there is good reason to stop using this term and consider instead the concept of secondary myocardial injury that relates to the underlying pathophysiology of the primary clinical condition

Splenic infarction: an update on William Osler\u27s observations.

BACKGROUND: Osler taught that splenic infarction presents with left upper abdominal quadrant pain, tenderness and swelling accompanied by a peritoneal friction rub. Splenic infarction is classically associated with bacterial endocarditis and sickle cell disease. OBJECTIVES: To describe the contemporary experience of splenic infarction. METHODS: We conducted a chart review of inpatients diagnosed with splenic infarction in a Jerusalem hospital between 1990 and 2003. RESULTS: We identified 26 cases with a mean age of 52 years. Common causes were hematologic malignancy (six cases) and intracardiac thrombus (five cases). Only three cases were associated with bacterial endocarditis. In 21 cases the splenic infarction brought a previously undiagnosed underlying disease to attention. Only half the subjects complained of localized left-sided abdominal pain, 36% had left-sided abdominal tenderness; 31% had no signs or symptoms localized to the splenic area, 36% had fever, 56% had leukocytosis and 71% had elevated lactate dehydrogenase levels. One splenectomy was performed and all patients survived to discharge. A post hoc analysis demonstrated that single infarcts were more likely to be associated with fever (20% vs. 63%, p \u3c 0.05) and leukocytosis (75% vs. 33%, P = 0.06) CONCLUSIONS: The clinical presentation of splenic infarction in the modern era differs greatly from the classical teaching, regarding etiology, signs and symptoms. In patients with unexplained splenic infarction, investigation frequently uncovers a new underlying diagnosis

Which diagnostic tests are most useful in a chest pain unit protocol?

Background The chest pain unit (CPU) provides rapid diagnostic assessment for patients with acute, undifferentiated chest pain, using a combination of electrocardiographic (ECG) recording, biochemical markers and provocative cardiac testing. We aimed to identify which elements of a CPU protocol were most diagnostically and prognostically useful. Methods The Northern General Hospital CPU uses 2–6 hours of serial ECG / ST segment monitoring, CK-MB(mass) on arrival and at least two hours later, troponin T at least six hours after worst pain and exercise treadmill testing. Data were prospectively collected over an eighteen-month period from patients managed on the CPU. Patients discharged after CPU assessment were invited to attend a follow-up appointment 72 hours later for ECG and troponin T measurement. Hospital records of all patients were reviewed to identify adverse cardiac events over the subsequent six months. Diagnostic accuracy of each test was estimated by calculating sensitivity and specificity for: 1) acute coronary syndrome (ACS) with clinical myocardial infarction and 2) ACS with myocyte necrosis. Prognostic value was estimated by calculating the relative risk of an adverse cardiac event following a positive result. Results Of the 706 patients, 30 (4.2%) were diagnosed as ACS with myocardial infarction, 30 (4.2%) as ACS with myocyte necrosis, and 32 (4.5%) suffered an adverse cardiac event. Sensitivities for ACS with myocardial infarction and myocyte necrosis respectively were: serial ECG / ST segment monitoring 33% and 23%; CK-MB(mass) 96% and 63%; troponin T (using 0.03 ng/ml threshold) 96% and 90%. The only test that added useful prognostic information was exercise treadmill testing (relative risk 6 for cardiac death, non-fatal myocardial infarction or arrhythmia over six months). Conclusion Serial ECG / ST monitoring, as used in our protocol, adds little diagnostic or prognostic value in patients with a normal or non-diagnostic initial ECG. CK-MB(mass) can rule out ACS with clinical myocardial infarction but not myocyte necrosis(defined as a troponin elevation without myocardial infarction). Using a low threshold for positivity for troponin T improves sensitivity of this test for myocardial infarction and myocardial necrosis. Exercise treadmill testing predicts subsequent adverse cardiac events

Diabetic Muscle Infarction

A 58-year-old male with past medical history of diabetes mellitus presented with pain to the bilateral groin for six weeks. Magnetic resonance imaging of the patient’s lower extremities revealed acute myoedema, and he was diagnosed with myositis secondary to diabetic muscle infarction

The effects of hourly differences in air pollution on the risk of myocardial infarction: case crossover analysis of the MINAP database.

OBJECTIVES: To investigate associations between air pollution levels and myocardial infarction (MI) on short timescales, with data at an hourly temporal resolution. DESIGN: Time stratified case crossover study linking clinical data from the Myocardial Ischaemia National Audit Project (MINAP) with PM(10), ozone, CO, NO(2), and SO(2) data from the UK National Air Quality Archive. Pollution effects were investigated with delays (lags) of 1-6, 7-12, 13-18, 19-24, and 25-72 hours in both single and multi-pollutant models, adjusted for ambient temperature, relative humidity, circulating levels of influenza and respiratory syncytial virus, day of week, holidays, and residual seasonality within calendar month strata. SETTING: Population based study in 15 conurbations in England and Wales. SUBJECTS: 79,288 diagnoses of myocardial infarction recorded over the period 2003-6. MAIN OUTCOME MEASURES: Excess risk of myocardial infarction per 10 µg/m(3) increase in pollutant level. RESULTS: In single pollutant models, PM(10) and NO(2) levels were associated with a very short term increase in risk of myocardial infarction 1-6 hours later (excess risks 1.2% (95% confidence interval 0.3 to 2.1) and 1.1% (0.3 to 1.8) respectively per 10 μg/m(3) increase); the effects persisted in multi-pollutant models, though with only weak evidence of an independent PM(10) effect (P = 0.05). The immediate risk increases were followed by reductions in risk at longer lags: we found no evidence of any net excess risk associated with the five pollutants studied over a 72 hour period after exposure. CONCLUSIONS: Higher levels of PM(10) and NO(2), which are typically markers of traffic related pollution, seem to be associated with transiently increased risk of myocardial infarction 1-6 hours after exposure, but later reductions in risk suggest that air pollution may be associated with bringing events forward in time ("short-term displacement") rather than increasing overall risk. The well established effect of air pollution on cardiorespiratory mortality may not be mediated through increasing the acute risk of myocardial infarction, but through another mechanism

Angiogenesis and Vasculogenesis at 7-Day of Reperfused Acute Myocardial Infarction

Objectives 
This study is to investigate the angiogenesis and vasculogenesis at the first week of reperfused acute myocardial infarction (AMI).
Methods 
16 of mini-swines (20 to 30 Kg) were randomly assigned to the sham-operated group and the AMI group. The acute myocardial infarction and reperfusion model was created and the pig tail catheter was performed to monitor hemodynamics before left anterior descending coronary artery (LAD) occlusion, 90 min of LAD occlusion and 120 min of LAD reperfusion. Pathologic myocardial tissue was collected at 7-day of LAD reperfusion and further assessed by immunochemistry, dual immunochemistry, in-situ hybridization, real-time quantitative polymerase chain reaction and western blot. 
Results 
The infarcted area had higher FLK1 mRNA expression than sham-operated area and the normal area (all P<0.05), and the infarcted and marginal areas showed higher CD146 protein expression than the sham-operated area (all P<0.05), but the microvessel density (CD31 positive expression of microvessels/HP) was not significantly different between the infarcted area and the sham-operated area (8.92±3.05 vs 6.43±1.54) at 7-day of reperfused acute myocardial infarction (P>0.05). 
Conclusions 
FLK1 and CD146 expression significantly increase in the infarcted and marginal areas, and the microvessel density is not significantly different between the infarcted area and the sham-operated area, suggesting that angiogenesis and vasculogenesis in the infarcted area appear to high frequency of increase in 7-day of reperfused myocardial infarction. 
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Diagnostic accuracy of 3.0-T magnetic resonance T1 and T2 mapping and T2-weighted dark-blood imaging for the infarct-related coronary artery in Non-ST-segment elevation myocardial infarction

Background: Patients with recent non–ST‐segment elevation myocardial infarction commonly have heterogeneous characteristics that may be challenging to assess clinically. Methods and Results: We prospectively studied the diagnostic accuracy of 2 novel (T1, T2 mapping) and 1 established (T2‐weighted short tau inversion recovery [T2W‐STIR]) magnetic resonance imaging methods for imaging the ischemic area at risk and myocardial salvage in 73 patients with non–ST‐segment elevation myocardial infarction (mean age 57±10 years, 78% male) at 3.0‐T magnetic resonance imaging within 6.5±3.5 days of invasive management. The infarct‐related territory was identified independently using a combination of angiographic, ECG, and clinical findings. The presence and extent of infarction was assessed with late gadolinium enhancement imaging (gadobutrol, 0.1 mmol/kg). The extent of acutely injured myocardium was independently assessed with native T1, T2, and T2W‐STIR methods. The mean infarct size was 5.9±8.0% of left ventricular mass. The infarct zone T1 and T2 times were 1323±68 and 57±5 ms, respectively. The diagnostic accuracies of T1 and T2 mapping for identification of the infarct‐related artery were similar (P=0.125), and both were superior to T2W‐STIR (P<0.001). The extent of myocardial injury (percentage of left ventricular volume) estimated with T1 (15.8±10.6%) and T2 maps (16.0±11.8%) was similar (P=0.838) and moderately well correlated (r=0.82, P<0.001). Mean extent of acute injury estimated with T2W‐STIR (7.8±11.6%) was lower than that estimated with T1 (P<0.001) or T2 maps (P<0.001). Conclusions: In patients with non–ST‐segment elevation myocardial infarction, T1 and T2 magnetic resonance imaging mapping have higher diagnostic performance than T2W‐STIR for identifying the infarct‐related artery. Compared with conventional STIR, T1 and T2 maps have superior value to inform diagnosis and revascularization planning in non–ST‐segment elevation myocardial infarction. Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT02073422