Effect of hypothermia therapy after outpatient cardiac arrest due to ventricular fibrillation.

BACKGROUND: Several investigators have emphasized the positive effect of hypothermia therapy on patients who have suffered from cardiac arrest. Salvaging patients from circulatory collapse is a pivotal task, but it is unclear whether additional hypothermia can practically contribute to an improvement in the neurological outcome. METHODS AND RESULTS: Since December 2005, our hospital has been using hypothermia therapy. Forty-six comatose patients after recovery of spontaneous circulation were consecutively enrolled in the present study. Twenty-five of the enrolled patients received hypothermia therapy and 21 did not because they were treated prior to 2005. The time from collapse to spontaneous circulation (P=0.09), the rates of performance of bystander CPR (P=0.370) and presence of a witnessed collapse (P=0.067) were not significantly different between the recovery group (n=28) and the non-recovery group (n=18). The additional hypothermia therapy was an independent predictor of neurological recovery (P=0.005, OR 6.5, 95%CI 1.74-24.27). The recovery rate was significantly higher in patients who received hypothermia therapy (80%) compared to those who did not (38%). CONCLUSIONS: Hypothermia therapy is very useful for treating patients who have had an out-of-hospital cardiac arrest; it should be induced rapidly and smoothly.

Increased serum anandamide level at ruptured plaque site in patients with acute myocardial infarction.

Inflammation caused by activated macrophages and T lymphocytes may trigger plaque rapture in acute coronary syndrome (ACS). Anandamide and 2-arachidonylglycerol (2-AG) are macrophage-derived signal lipids and may be involved in the pathogenesis of ACS, but no clinical relevant data have been reported. In 43 acute myocardial infarction (AMI) patients (66 +/- 2 years), blood samples were obtained from the aortic root and the infarct-related coronary artery (IRA) using a PercuSurge system during primary percutaneous coronary intervention (PCI). In six patients with stable effort angina (SEA) (56 +/- 6 years), blood samples were obtained from the site of stenosis during elective PCI. In 25 of the 43 AMI patients, anandamide was detected in the serum. Serum anandamide level was 35 +/- 20 pmol/mL in the aorta and was significantly increased to 401 +/- 134 pmol/mL in the IRA (P < 0.01). 2-AG was undetectable in most of the patients. In patients with SEA, neither anandamide nor 2-AG was detected in the serum at the plaque site. In AMI patients with anandamide detected, left ventricular ejection fraction at 2 weeks after PCI was increased by 3.7 +/- 2.1% compared with that at the acute phase, while it was decreased by 3.0 +/- 1.8% in those without anandamide detected (P < 0.05). The serum anandamide level at the culprit lesion was elevated compared with the systemic level in a significant number of AMI patients, indicating the synthesis of anandamide at the IRA. Anandamide was suggested to be derived from ruptured plaque and may exert beneficial effects in humans.

Feasibility and safety of thrombectomy with TVAC aspiration catheter system for patients with acute myocardial infarction.

Early reperfusion with angioplasty and stenting is established as a central, effective treatment for acute myocardial infarction (AMI). The role of thrombectomy prior to angioplasty remains to be elucidated. To evaluate its feasibility, safety, and efficacy, thrombectomy using a TVAC aspiration catheter system was attempted prior to angioplasty and stenting in 40 consecutive patients with AMI. Fifty consecutive patients with AMI in whom angioplasty and stenting were performed without prior thrombectomy served as controls. Neither distribution of Killip classification nor culprit lesion was different between the two groups. In patients treated with the TVAC system, the procedure was successful in 39/40 patients (98%) and there were no procedure-related complications. In the final coronary angiogram, TIMI-3 (Thrombolysis in Myocardial Infarction) flow was obtained in 37/40 (93%) in patients treated with the TVAC system and 43/50 (86%) in control patients. Electrocardiograms before and after coronary intervention were analyzed in patients with ST elevation AMI (35 patients treated with the TVAC system and 41 control patients). ST elevation recovery >50% of the initial value was observed after coronary intervention in 26/35 (74%) in patients treated with the TVAC system and 26/41 (63%) in control patients (P = 0.33). In the case of anterior AMI, ST elevation recovery >50% of the initial value was observed in 13/17 (76%) in patients treated with the TVAC system and 8/20 (40%) in control patients (P = 0.045). Thus, thrombectomy using a TVAC system is feasible, safe, and may have the potential to enhance ST-segment resolution in patients with anterior AMI.

Enalapril suppresses ventricular remodeling more effectively than losartan in patients with acute myocardial infarction.

BACKGROUND: Ventricular remodeling after acute myocardial infarction (AMI) is associated with increased morbidity and mortality. ELITE II study showed that losartan, an angiotensin receptor blocker, shows a survival benefit to the same degree as captopril, an angiotensin-converting enzyme inhibitor, does in patients with heart failure. However, recent OPTIMAAL study showed that clinical outcomes after losartan are not superior to those after captopril in patients with AMI. We examined the effect of losartan on ventricular remodeling after AMI comparatively with that of enalapril. METHODS: We enrolled 203 consecutive patients with AMI (mean age 62 +/- 11 years). All patients underwent primary percutaneous coronary intervention and were randomly assigned to losartan (25-50 mg, n = 101) or enalapril (2.5-10 mg, n = 102) treatment. Biplane left ventriculography was performed just after primary percutaneous transluminal coronary angioplasty (acute phase) and 6 months after the onset of AMI. RESULTS: Any of the maximal creatine kinase level, left ventricular end-diastolic volume index, end-systolic volume index, and ejection fraction measured at acute phase was not different between losartan and enalapril groups. However, changes in left ventricular end-diastolic index (18 +/- 25 vs 8 +/- 24 mL/m2) and left ventricular end-systolic volume index (10 +/- 20 vs 2 +/- 18 mL/m2) from acute phase to 6 months were significantly greater in losartan than in enalapril group. Change in left ventricular ejection fraction (0.2% +/- 10.3% vs 3.4% +/- 11.6%) from acute phase to 6 months was significantly smaller in losartan than in enalapril group. The plasma level of brain natriuretic peptide at 6 months was significantly higher in losartan than in enalapril group (all P < .05). CONCLUSION: These indicate that enalapril suppresses ventricular remodeling after AMI more effectively than losartan.