Contact-to-balloon time and door-to-balloon time after initiation of a formalized data feedback in patients with acute ST-elevation myocardial infarction.

For many patients with ST-segment elevation myocardial infarctions (STEMIs), the time from presentation to percutaneous coronary intervention exceeds established goals. This study was conducted to examine the effects of formalized data assessment and systematic feedback on treatment times. All patients with STEMIs treated with percutaneous coronary intervention in a semi-rural 3-hospital network from January 1, 2006, to December 31, 2006, were prospectively analyzed (n = 114). Patients presenting during the first 3-month period (January 1, 2006, to March 31, 2006) were included as the reference group (n = 33). Time points from initial contact with the medical system to revascularization were assessed, analyzed, and presented in an interactive session to hospital and emergency services staff members. Data from patients with STEMIs presenting during the next 3 quarters were presented in the same manner (n = 28, 25, and 28). The median contact-to-balloon time was 113 minutes in the reference quarter, decreasing to 83, 66, and 74 minutes in the intervention groups (p <0.0001), whereas the median door-to-balloon time decreased from 54 minutes in the reference group to 35, 31, and 26 minutes in the intervention groups (p <0.0001). The proportion of patients with contact-to-balloon times <90 minutes increased from 21% to 79% (p <0.0001). There were significant reductions in the durations of initial treatment on location and in the emergency room and in puncture-to-balloon-time in the catheterization laboratory, and more patients were transported directly to the catheterization laboratory, bypassing the emergency room (from 23% in the reference quarter to 76% in the last intervention quarter, p <0.0001). In conclusion, formalized data feedback leads to marked reduction in revascularization times in patients with STEMIs.

Hydroxyl radical-induced acute diastolic dysfunction is due to calcium overload via reverse-mode Na(+)-Ca(2+) exchange.

Hydroxyl radicals (OH) are involved in the development of reperfusion injury and myocardial failure. In the acute phase of the OH-mediated diastolic dysfunction, increased intracellular Ca(2+) levels and alterations of myofilaments may play a role, but the relative contribution of these systems to myocardial dysfunction is unknown. Intact contracting cardiac trabeculae from rabbits were exposed to OH, resulting in an increase in diastolic force (F(dia)) by 540%. Skinned fiber experiments revealed that OH-exposed preparations were sensitized for Ca(2+) (EC(50): 3.27+/-0.24 x 10(-6) versus 2.69+/-0.15 x 10(-6) mol/L; P<0.05), whereas maximal force development was unaltered. Western blots showed a proteolytic degradation of troponin T (TnT) with intact troponin I (TnI). Blocking of calpain I by MDL-28.170 inhibited both TnT-proteolysis and Ca(2+) sensitization, but failed to prevent the acute diastolic dysfunction in the intact preparation. The OH-induced diastolic dysfunction was similar in preparations with intact (540+/-93%) and pharmacologically blocked sarcoplasmic reticulum (539+/-77%), and was also similar in presence of the L-type Ca(2+)-channel antagonist verapamil. In sharp contrast, inhibition of the reverse-mode sodium-calcium exchange by KB-R7943 preserved diastolic function completely. Additional experiments were performed in rat myocardium; the rise in diastolic force was comparable to rabbit myocardium, but Ca(2+) sensitivity was unchanged and maximal force development was reduced. This was associated with a degradation of TnI, but not TnT. Electron microscopic analysis revealed that OH did not cause irreversible membrane damage. We conclude that OH-induced acute diastolic dysfunction is caused by Ca(2+) influx via reverse mode of the sodium-calcium exchanger. Degradation of troponins appears to be species-dependent but does not contribute to the acute diastolic dysfunction.

[Tako-tsubo cardiomyopathy. Incidence in patients with acute coronary syndrome]. / Tako-Tsubo-Kardiomyopathie. Inzidenz bei Patienten mit akutem Koronarsyndrom.

BACKGROUND AND METHODS: In 2005, an emergency coronary angiography was performed at the authors' clinic in 215 patients (148 men, 67 women) with troponin-positive acute coronary syndrome. RESULTS: In five of these patients (exclusively women, mean age [+/- SD] 61 +/- 12 years), tako-tsubo cardiomyopathy was identified. This represents a frequency of 2.3% (5/215 patients) of all investigated patients and of 7.5% (5/67 patients) within the group of women. In these patients, levocardiography revealed severe left ventricular dysfunction with apical wall motion abnormality known as "apical ballooning". At angiography, a significant coronary artery disease could be excluded. Chest pain was present in all patients, combined with ST segment elevation in one (20%) and T-wave inversion in four (80%). Elevated cardiac markers were found in all cases. All patients experienced psychologically stressful circumstances preceding the onset of symptoms. The patients all survived, showing normalized ejection fraction and rapid restoration of previous cardiovascular function within a mean (+/- SD) of 15 +/- 11 days. CONCLUSION: Tako-tsubo cardiomyopathy is a distinctive form of regional left ventricular dysfunction triggered by psychologically stressful events, which has a favorable clinical outcome. With a remarkable frequency of 7.5% especially in women, tako-tsubo cardiomyopathy should be included in the differential diagnosis of acute myocardial infarction.