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The Frank-Starling 'law of the heart' is implicated in certain types of orthostatic intolerance in humans. Environmental conditions have the capacity to modulate orthostatic tolerance, where heat stress decreases and cooling increases orthostatic tolerance. The objective of this project was to test the hypothesis that heat stress augments and cooling attenuates orthostatic-induced decreases in stroke volume (SV) via altering the operating position on a Frank-Starling curve. Pulmonary artery catheters were placed in 11 subjects for measures of pulmonary capillary wedge pressure (PCWP) and SV (thermodilution derived cardiac output/heart rate). Subjects experienced lower-body negative-pressure (LBNP) of 0, 15 and 30 mmHg during normothermia, skin-surface cooling (decrease in mean skin temperature of 4.3 ± 0.4• C (mean ± s.e.m.) via perfusing 16• C water through a tubed-lined suit), and whole-body heating (increase in blood temperature of 1.0 ± 0.1• C via perfusing 46 • C water through the suit). SV was 123 ± 8, 121 ± 10, 131 ± 7 ml prior to LBNP, during normothermia, skin-surface cooling, and whole-body heating, respectfully (P = 0.20). LBNP of 30 mmHg induced greater decreases in SV during heating (−48.7 ± 6.7 ml) compared to normothermia (−33.2 ± 7.4 ml) and to cooling (−10.3 ± 2.9 ml; all P < 0.05). Relating PCWP to SV indicated that cooling values were located on the flatter portion of a Frank-Starling curve because of attenuated decreases in SV per decrease in PCWP. In contrast, heating values were located on the steeper portion of a Frank-Starling curve because of augmented decreases in SV per decrease in PCWP. These data suggest that a Frank-Starling mechanism may contribute to improvements in orthostatic tolerance during cold stress and orthostatic intolerance during heat stress.

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The implantable cardioverter defibrillator (ICD) is able to reduce sudden arrhythmic death in patients who are considered to be at high risk. However, the arrhythmic risk may be increased only temporarily as long as the proarrhythmic conditions persist, left ventricular ejection fraction remains low, or heart failure prevails. The wearable cardioverter defibrillator (WCD) represents an alternative approach to prevent sudden arrhythmic death until either ICD implantation is clearly indicated or the arrhythmic risk is considered significantly lower or even absent. The WCD is also indicated for interrupted protection by an already implanted ICD, temporary inability to implant an ICD, and lastly refusal of an indicated ICD by the patient. The WCD is not an alternative to the ICD, but a device that may contribute to better selection of patients for ICD therapy. The WCD has the characteristics of an ICD, but does not need to be implanted, and it has similarities with an external defibrillator, but does not require a bystander to apply lifesaving shocks when necessary. The WCD was introduced into clinical practice about 8 years ago, and indications for its use are currently expanding. This article describes the technological aspects of the WCD, discusses current indications for its use, and reviews the clinical studies with the WCD. Additionally, data are reported on the clinical experience with the WCD based on 354 patients from Germany hospitalized between 2000 and 2008 who wore the WCD for a mean of 3 months.

for the Cardiac Arrhythmias and Risk Stratification After Acute Myocardial Infarction (CARISMA) Study Group Background-Knowledge about the incidence of cardiac arrhythmias after acute myocardial infarction has been limited by the lack of traditional ECG recording systems to document and confirm asymptomatic and symptomatic arrhythmias. The Cardiac Arrhythmias and Risk Stratification After Myocardial Infarction (CARISMA) trial was designed to study the incidence and prognostic significance of arrhythmias documented by an implantable cardiac monitor among patients with acute myocardial infarction and reduced left ventricular ejection fraction. Methods and Results-A total of 1393 of 5869 patients (24%) screened in the acute phase (3 to 21 days) of an acute myocardial infarction had left ventricular ejection fraction Յ40%. After exclusions, 297 patients (21%) (meanϮSD age, 64.0Ϯ11.0 years; left ventricular ejection fraction, 31Ϯ7%) received an implantable cardiac monitor within 11Ϯ5 days of the acute myocardial infarction and were followed up every 3 months for an average of 1.9Ϯ0.5 years. Predefined bradyarrhythmias and tachyarrhythmias were recorded in 137 patients (46%); 86% of these were asymptomatic. The implantable cardiac monitor documented a 28% incidence of new-onset atrial fibrillation with fast ventricular response (Ն125 bpm), a 13% incidence of nonsustained ventricular tachycardia (Ն16 beats), a 10% incidence of high-degree atrioventricular block (Յ30 bpm lasting Ն8 seconds), a 7% incidence of sinus bradycardia (Յ30 bpm lasting Ն8 seconds), a 5% incidence of sinus arrest (Ն5 seconds), a 3% incidence of sustained ventricular tachycardia, and a 3% incidence of ventricular fibrillation. Cox regression analysis with time-dependent covariates revealed that high-degree atrioventricular block was the most powerful predictor of cardiac death (hazard ratio, 6.75; 95% confidence interval, 2.55 to 17.84; PϽ0.001). Conclusions-This is the first study to report on long-term cardiac arrhythmias recorded by an implantable loop recorder in patients with left ventricular ejection fraction Յ40% after myocardial infarction. Clinically significant bradyarrhythmias and tachyarrhythmias were documented in a substantial proportion of patients with depressed left ventricular ejection fraction after acute myocardial infarction. Intermittent high-degree atrioventricular block was associated with a very high risk of cardiac death. Clinical Trial Registration-URL: http://www.ClinicalTrials.gov, Unique identifier: NCT00145119.