Cardiac atrial cells lack a regular system of transverse tubules like that in cardiac ventricular cells. Nevertheless, many atrial cells do possess an irregular internal transverse‐axial tubular system (TATS). To investigate the possible role of the TATS in excitation‐contraction coupling in atrial myocytes, we visualized the TATS (labelled with the fluorescent indicator, Di‐8‐ANEPPS) simultaneously with Ca2+ transients and/or Ca2+ sparks (fluo‐4). In confocal transverse linescan images of field‐stimulated cells, whole‐cell Ca2+ transients had two morphologies: ‘U‐shaped’ transients and irregular or ‘W‐shaped’ transients with a varying number of points of origin of the Ca2+ transient. About half (54 %, n=289 cells, 13 animals) of the cells had a TATS. Cells with TATS had a larger mean diameter (13.2 ± 2.8 μm) than cells without TATS (11.7 ± 2.0 μm) and were more common in the left atrium (n= 206 cells; left atrium: 76 with TATS, 30 without TATS; right atrium: 42 with TATS, 58 without TATS). Simultaneous measurement of Ca2+ sparks and sarcolemmal structures showed that cells without TATS had U‐shaped transients that started at the cell periphery, and cells with TATS had W‐shaped transients that began simultaneously at the cell periphery and the TATS. Most (82 out of 102 from 31 cells) ‘spontaneous’ (non‐depolarized) Ca2+ sparks occurred within 1 μm of a sarcolemmal structure (cell periphery or TATS), and 33 % occurred within 1 pixel (0.125 μm). We conclude that the presence of a sarcolemmal membrane either at the cell periphery or in the TATS in close apposition to the sarcoplasmic reticulum is required for the initiation of an evoked Ca2+ transient and for spontaneous Ca2+ sparks.

Background-Delivery of inappropriate shocks caused by misdetection of supraventricular tachycardia (SVT) remains a substantial complication of implanted cardioverter/defibrillator (ICD) therapy. Whether use of optimally programmed dual-chamber ICDs lowers this risk compared with that in single-chamber ICDs is not clear. Methods and Results-Subjects with a clinical indication for ICD (nϭ400) at 27 participating centers received dual-chamber ICDs and were randomly assigned to strictly defined optimal single-or dual-chamber detection in a single-blind manner. Programming minimized ventricular pacing. The primary end point was the proportion of SVT episodes inappropriately detected from the time of programming until crossover or end of study. On a per-episode basis, 42% of the episodes in the single-chamber arm and 69% of the episodes in the dual-chamber arm were due to SVT. Mortality (3.5% in both groups) and early study withdrawal (14% single-chamber, 11% dual-chamber) were similar in both groups. The rate of inappropriate detection of SVT was 39.5% in the single-chamber detection arm compared with 30.9% in the dual-chamber arm.

Abstract-To investigate the cellular mechanisms for altered Ca 2ϩ homeostasis and contractility in cardiac hypertrophy, we measured whole-cell L-type Ca 2ϩ currents (I Ca,L ), whole-cell Ca 2ϩ transients ([Ca 2ϩ ] i ), and Ca 2ϩ sparks in ventricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age-and sex-matched Wistar-Kyoto and Sprague-Dawley control rats. By echocardiography, SHR hearts had cardiac hypertrophy and enhanced contractility (increased fractional shortening) and no signs of heart failure. C ardiac hypertrophy is associated with marked changes in myocardial contractility. Peak active tension increases, 1-4 and the rates of both contraction and relaxation are slowed. 3,[5][6][7][8] These contractile abnormalities are associated with alterations in the whole-cell calcium transient ([Ca 2ϩ ] i ). In the hypertrophied myocardium, the amplitude of [Ca 2ϩ ] i increases, 9 whereas in failing myocardium, the amplitude of [Ca 2ϩ ] i decreases. 10 -13 In most animal models of hypertrophy 8,10,11,[13][14][15] and in failing human hearts, 12,16 the duration of the whole-cell [Ca 2ϩ ] i is also prolonged. However, the precise cellular mechanisms that are responsible for changes in contractility and alterations in [Ca 2ϩ ] i are largely unknown. Identification of the cellular mechanisms that underlie altered excitation-contraction coupling in cardiac hypertrophy and heart failure is complicated by several issues, including differences in experimental animal models and disease progression. In addition, it has only recently proved possible using confocal microscopy to measure local nonpropagating elevations of Ca 2ϩ (Ca 2ϩ sparks) at the level of individual sarcomeres. [17][18][19][20][21][22] The ability to measure Ca 2ϩ sparks provides an opportunity to evaluate directly the role of sarcoplasmic reticulum (SR) Ca 2ϩ release in muscle cells from animal models associated with cardiac hypertrophy.In this study, we used laser scanning confocal microscopy and Ca 2ϩ -sensitive fluorescent indicators to detect Ca 2ϩ sparks evoked by electrical field stimulation in ventricular cells from normal rats and from spontaneously hypertensive rats (SHRs) with cardiac hypertrophy. By quantitative analysis of the kinetic characteristics of Ca 2ϩ sparks, we identify enhanced SR Ca 2ϩ release from hypertrophied SHR cells. In