BackgroundLimited information is available on the contemporary and potentially changing trends in the incidence, management, and outcomes of cardiogenic shock complicating ST‐elevation myocardial infarction (STEMI).Methods and ResultsWe queried the 2003–2010 Nationwide Inpatient Sample databases to identify all patients ≥40 years of age with STEMI and cardiogenic shock. Overall and age‐, sex‐, and race/ethnicity‐specific trends in incidence of cardiogenic shock, early mechanical revascularization, and intra‐aortic balloon pump use, and inhospital mortality were analyzed. From 2003 to 2010, among 1 990 486 patients aged ≥40 years with STEMI, 157 892 (7.9%) had cardiogenic shock. The overall incidence rate of cardiogenic shock in patients with STEMI increased from 6.5% in 2003 to 10.1% in 2010 (Ptrend<0.001). There was an increase in early mechanical revascularization (30.4% to 50.7%, Ptrend<0.001) and intra‐aortic balloon pump use (44.8% to 53.7%, Ptrend<0.001) in these patients over the 8‐year period. Inhospital mortality decreased significantly, from 44.6% to 33.8% (Ptrend<0.001; adjusted OR, 0.71; 95% CI, 0.68 to 0.75), whereas the average total hospital cost increased from $35 892 to $45 625 (Ptrend<0.001) during the study period. There was no change in the average length of stay (Ptrend=0.394). These temporal trends were similar in patients <75 and ≥75 years of age, men and women, and across each racial/ethnic group.ConclusionsThe incidence of cardiogenic shock complicating STEMI has increased during the past 8 years together with increased use of early mechanical revascularization and intra‐aortic balloon pumps. There has been a concomitant decrease in risk‐adjusted inhospital mortality, but an increase in total hospital costs during this period.

Enhanced external counterpulsation reduces angina and extends time to exercise-induced ischemia in patients with symptomatic CAD. Treatment was relatively well tolerated and free of limiting side effects in most patients.

Background-Observational studies have suggested that psychological stress increases the incidence of sudden cardiac death. Whether emotional or physical stressors can trigger spontaneous ventricular arrhythmias in patients at risk has not been systematically evaluated. Methods and Results-Patients with implantable cardioverter-defibrillators (ICDs) were given diaries to record levels of defined mood states and physical activity, using a 5-point intensity scale, during 2 periods preceding spontaneously occurring ICD shocks (0 to 15 minutes and 15 minutes to 2 hours) and during control periods 1 week later. ICD-stored electrograms confirmed the rhythm at the time of shock. A total of 107 confirmed ventricular arrhythmias requiring shock were reported by 42 patients (33 men; mean age, 65 years; 78% had coronary artery disease) between August 1996 and September 1999. In the 15 minutes preceding shock, an anger level Ն3 preceded 15% of events compared with 3% of control periods (PϽ0.04; odds ratio, 1.83; 95% confidence intervals, 1.04 to 3.16) Other mood states (anxiety, worry, sadness, happiness, challenge, feeling in control, or interest) did not differ. Patients were more physically active preceding shock than in control periods. Anger and physical activity were independently associated with the preshock period. Conclusions-Anger and physical activity can trigger ventricular arrhythmias in patients with ICDs. Future investigations of therapies aimed at blocking a response to these stressors may decrease ventricular arrhythmias and shocks in these

BackgroundThe reported incidence of peripartum cardiomyopathy (PPCM) in the United States varies widely. Furthermore, limited information is available on the temporal trends in incidence and outcomes of PPCM.Methods and ResultsWe queried the 2004‐2011 Nationwide Inpatient Sample databases to identify all women aged 15 to 54 years with the diagnosis of PPCM. Temporal trends in incidence (per 10 000 live births), maternal major adverse events (MAE; defined as in‐hospital mortality, cardiac arrest, heart transplant, mechanical circulatory support, acute pulmonary edema, thromboembolism, or implantable cardioverter defibrillator/permanent pacemaker implantation), cardiogenic shock, and mean length of stay were analyzed. From 2004 to 2011, we identified 34 219 women aged 15 to 54 years with PPCM. The overall PPCM rate was 10.3 per 10 000 (or 1 in 968) live births. PPCM incidence increased from 8.5 to 11.8 per 10 000 live births (Ptrend<0.001) over the past 8 years. MAE occurred in 13.5% of patients. There was no temporal change in MAE rate, except a small increase in in‐hospital mortality and mechanical circulatory support (Ptrend<0.05). Cardiogenic shock increased from 1.0% in 2004 to 4.0% in 2011 (Ptrend<0.001). Mean length of stay decreased during the study period.ConclusionFrom 2004 to 2011, the incidence of PPCM has increased in the United States. Maternal MAE rates overall have remained unchanged while cardiogenic shock, utilization of mechanical circulatory support, and in‐hospital mortality have increased during the study period. Further study of the mechanisms underlying these adverse trends in the incidence and outcomes of PPCM are warranted.

No abstract

Heart transplant rejection is characterized pathologically by myocyte necrosis and apoptosis associated with interstitial mononuclear cell infiltration. Any one of these components can be targeted for noninvasive detection of transplant rejection. During apoptotic cell death, phosphatidylserine, a phospholipid that is normally confined to the inner leaflet of cell membrane bilayer, gets exteriorized. Technetium-99m-labeled annexin-V, an endogenous protein that has high affinity for binding to phosphatidylserine, has been administered intravenously for noninvasive identification of apoptotic cell death. In the present study of 18 cardiac allograft recipients, 13 patients had negative and five had positive myocardial uptake of annexin. These latter five demonstrated at least moderate transplant rejection and caspase-3 staining, suggesting apoptosis in their biopsy specimens. This study reveals the clinical feasibility and safety of annexin-V imaging for noninvasive detection of transplant rejection by targeting cell membrane phospholipid alterations that are commonly associated with the process of apoptosis.

Patients with coronary artery disease and mental stress-provoked silent ventricular dysfunction were distinguished by a psychological profile consistent with emotional reactivity to social interaction and mental provocation, with anger as the predominant affective state. Patients with such a profile may be at risk of frequent silent left ventricular dysfunction.

Cardiac hemochromatosis or primary iron-overload cardiomyopathy is an important and potentially preventable cause of heart failure. This is initially characterized by diastolic dysfunction and arrhythmias and in later stages by dilated cardiomyopathy. Diagnosis of iron overload is established by elevated transferrin saturation (>55%) and elevated serum ferritin (>300 ng/mL). Genetic testing for mutations in the HFE (high iron) gene and other proteins, such as hemojuvelin, transferrin receptor, and ferroportin, should be performed if secondary causes of iron overload are ruled out. Patients should undergo comprehensive 2D and Doppler echocardiography to evaluate their systolic and diastolic function. Newer modalities like strain imaging and speckle-tracking echocardiography hold promise for earlier detection of cardiac involvement. Cardiac magnetic resonance imaging with measurement of T2* relaxation times can help quantify myocardial iron overload. In addition to its value in diagnosis of cardiac iron overload, response to iron reduction therapy can be assessed by serial imaging. Therapeutic phlebotomy and iron chelation are the cornerstones of therapy. The average survival is less than a year in untreated patients with severe cardiac impairment. However, if treated early and aggressively, the survival rate approaches that of the regular heart failure population.