European Practice Assessment of Cardiovascular risk management (EPA Cardio): protocol of an international observational study in primary care

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Mild hypothermia delays the development of stone heart from untreated sustained ventricular fibrillation - a cardiovascular magnetic resonance study

<p>Abstract</p> <p>Background</p> <p>'Stone heart' resulting from ischemic contracture of the myocardium, precludes successful resuscitation from ventricular fibrillation (VF). We hypothesized that mild hypothermia might slow the progression to stone heart.</p> <p>Methods</p> <p>Fourteen swine (27 ± 1 kg) were randomized to normothermia (group I; n = 6) or hypothermia groups (group II; n = 8). Mild hypothermia (34 ± 2°C) was induced with ice packs prior to VF induction. The LV and right ventricular (RV) cross-sectional areas were followed by cardiovascular magnetic resonance until the development of stone heart. A commercial 1.5T GE Signa NV-CV/i scanner was used. Complete anatomic coverage of the heart was acquired using a steady-state free precession (SSFP) pulse sequence gated at baseline prior to VF onset. Un-gated SSFP images were obtained serially after VF induction. The ventricular endocardium was manually traced and LV and RV volumes were calculated at each time point.</p> <p>Results</p> <p>In group I, the LV was dilated compared to baseline at 5 minutes after VF and this remained for 20 minutes. Stone heart, arbitrarily defined as LV volume <1/3 of baseline at the onset of VF, occurred at 29 ± 3 minutes. In group II, there was less early dilation of the LV (p < 0.05) and the development of stone heart was delayed to 52 ± 4 minutes after onset of VF (P < 0.001).</p> <p>Conclusions</p> <p>In this closed-chest swine model of prolonged untreated VF, hypothermia reduced the early LV dilatation and importantly, delayed the onset of stone heart thereby extending a known, morphologic limit of resuscitability.</p

Machine Learning Techniques for the Detection of Shockable Rhythms in Automated External Defibrillators

Early recognition of ventricular fibrillation (VF) and electrical therapy are key for the survivalof out-of-hospital cardiac arrest (OHCA) patients treated with automated external defibrilla-tors (AED). AED algorithms for VF-detection are customarily assessed using Holter record-ings from public electrocardiogram (ECG) databases, which may be different from the ECGseen during OHCA events. This study evaluates VF-detection using data from both OHCApatients and public Holter recordings. ECG-segments of 4-s and 8-s duration were ana-lyzed. For each segment 30 features were computed and fed to state of the art machinelearning (ML) algorithms. ML-algorithms with built-in feature selection capabilities wereused to determine the optimal feature subsets for both databases. Patient-wise bootstraptechniques were used to evaluate algorithm performance in terms of sensitivity (Se), speci-ficity (Sp) and balanced error rate (BER). Performance was significantly better for publicdata with a mean Se of 96.6%, Sp of 98.8% and BER 2.2% compared to a mean Se of94.7%, Sp of 96.5% and BER 4.4% for OHCA data. OHCA data required two times morefeatures than the data from public databases for an accurate detection (6 vs 3). No signifi-cant differences in performance were found for different segment lengths, the BER differ-ences were below 0.5-points in all cases. Our results show that VF-detection is morechallenging for OHCA data than for data from public databases, and that accurate VF-detection is possible with segments as short as 4-s

Compliance characteristics of the human chest during cardiopulmonary resuscitation. Final report.

National Highway Traffic Safety Administration, Washington, D.C.Mode of access: Internet.Author corporate affiliation: Johns Hopkins Hospital, Cardiology Division, Baltimore, Md.Report covers the period April 1977-June 1979. Released Feb 1981. Contract amount $56,035Subject code: EASubject code: JNSubject code: NCKBSubject code: NLSFSubject code: OA

Hemodynamic determinants of the time-course of fall in canine left ventricular pressure.

The hemodynamic determinants of the time-course of fall in isovolumic left ventricular pressure were assessed in isolated canine left ventricular preparations. Pressure fall was studied in isovolumic beats or during prolonged isovolumic diastole after ejection. Pressure fall was studied in isovolumic relaxation for isovolumic and ejecting beats (r less than or equal to 0.98) and was therefore characterized by a time constant, T. Higher heart rates shortened T slightly from 52.6 +/- 4.5 ms at 110/min to 48.2 +/- 6.0 ms at 160/min (P less than 0.01, n = 8). Higher ventricular volumes under isovolumic conditions resulted in higher peak left ventricular pressure but no significant change in T. T did shorten from 67.1 +/- 5.0 ms in isovolumic beats to 45.8 +/- 2.9 ms in the ejecting beats (P less than 0.001, n = 14). In the ejecting beats, peak systolic pressure was lower, and end-systolic volume smaller. To differentiate the effects of systolic shortening during ejection from those of lower systolic pressure and smaller end-systolic volume, beats with large end-diastolic volumes were compared to beats with smaller end-diastolic volumes. The beats with smaller end-diastolic volumes exhibited less shortening but similar end-systolic volumes and peak systolic pressure. T again shortened to a greater extent in the beats with greater systolic shortening. Calcium chloride and acetylstrophanthidin resulted in no significant change in T, but norepinephrine, which accelerates active relaxation, resulted in a significant shortening of T (65.6 +/- 13.4 vs. 46.3 +/- 7.0 ms, P less than 0.02). During recovery from ischemia, T increased significantly from 59.3 +/- 9.6 to 76.8 +/- 13.1 ms when compared with the preischemic control beat (P less than 0.05). Thus, the present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate. T may be an index of the activity of the active cardiac relaxing system and appears dependent on systolic fiber shortening