To examine the effects of rapid dehydration on isometric muscular strength and endurance, seven men were tested at baseline (control) and after a dehydration (dHST) and a euhydration (eHST) heat stress trial. The dHST consisted of intermittent sauna exposure until 4% of body mass was lost, whereas the eHST consisted of intermittent sauna exposure (same duration as dHST) with water replacement. Peak torque was determined for the knee extensors and elbow flexors during three isometric maximal voluntary contractions. Time to fatigue was determined by holding a maximal voluntary contraction until torque dropped below 50% peak torque for 5 s. Strength and endurance were assessed 3.5 h after the HSTs (no food or water intake). Body mass was decreased 3.8+/-0.4% post dHST and 0.4+/-0.3% post eHST. Plasma volume was decreased 7.5+/-4.6% and 5.7+/-4.4%, 60 and 120 min post dHST, respectively. A small (1.6 mEq x L[-1]) but significant increase was found for serum Na+ concentration 60 min post dHST but had returned to predehydration level 120 min post dHST. Serum K+ and myoglobin concentrations were not affected by HSTs. Peak torque was not different (P > 0.05) among control, dHST, and eHST for the knee extensors (Mean (Nm)+/-SD, 285+/-79, 311+/-113, and 297+/-79) and elbow flexors (79+/-12, 83+/-15, and 80+/-12). Time to fatigue was not different (P > 0.05) among control, dHST and eHST for the knee extensors (Mean (s)+/-SD. 42.4+/-11.5, 45.3+/-7.6, and 41.8+/-6.0) and elbow flexors (48.2+/-8.9, 44.0+/-9.4, and 46.0+/-6.4). These results provide evidence that isometric strength and endurance are unaffected 3.5 h after dehydration of approximately 4% body mass.

Background-Induced external hypothermia during ventricular fibrillation (VF) improves resuscitation outcomes. Our objectives were twofold (1) to determine if very rapid hypothermia could be achieved by intrapulmonary administration of cold perfluorocarbons, thereby using the lungs as a vehicle for targeted cardiopulmonary hypothermia, and (2) to determine if this improved resuscitation success.

We describe a case of anterior mitral leaflet perforation successfully treated with the Amplatzer Cribriform device, with resultant hemolytic anemia. The device was retrieved, and perforation occluded with the GORE CARDIOFORM device with resolution of hemolysis. ( Level of Difficulty: Advanced. )

Background Mutations in the X-linked gene encoding dystrophin cause skeletal and cardiac muscle diseases in men. Female “carriers” also can develop overt disease. The purpose of this study was to ascertain the prevalence of cardiac contractile abnormalities in dystrophinopathy carriers. Methods Twenty-four dystrophinopathy heterozygotes and 24 normal women each underwent standard exercise stress echocardiography. Results Heterozygotes demonstrated mildly lower left ventricular ejection fractions (LVEFs) at rest compared with controls (0.56 ± 0.10 vs 0.62 ± 0.07, P = .02). After exercise, the mean LVEF fell to 0.53 ± 0.14 in heterozygotes but rose to 0.73 ± 0.07 in controls (P < .001). Twenty-one of 24 dystrophinopathy heterozygotes demonstrated ≥1 of the following: abnormal resting LVEF, abnormal LVEF response to exercise, or exercise-induced wall motion abnormality. Conclusions Women heterozygous for dystrophinopathy demonstrate significant left ventricular systolic dysfunction, which is unmasked by exercise. This finding has mechanistic implications for both inherited and acquired cardiac disease states.

Bioprosthetic valve thrombosis (BPVT) is not uncommon but can be under diagnosed due to the lack of awareness and technical limitations of echocardiography. When suspecting BPVT, it is imperative to consider multimodality imaging to establish the diagnosis as early treatment can alter the clinical course. Here we present a case series of two patients with a history of rheumatic heart disease status post bioprosthetic mitral valve replacement who presented with acute heart failure symptoms. In both cases, supplemental imaging with real-time 3D echocardiography was critical in establishing a diagnosis of BPVT, resulting in timely treatment. These cases support updating current guidelines for the management of patients with bioprosthetic valve replacement to include more frequent surveillance imaging even if patients are asymptomatic.