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The aim of this study was to determine whether defibrillation waveform duration adjustment with single-coil defibrillation leads can be used to increase the proportion of patients with satisfactory defibrillation thresholds (DFTs). A retrospective analysis of the DFT levels for 105 patients with implantable cardioverter-defibrillator devices and a single-coil defibrillation lead was performed. Two groups of patients were compared: 34 patients who had undergone waveform tuning (group A) and 71 patients with a fixed-tilt waveform (group B). Additional data including demographics, etiology, New York Heart Association functional class, left ventricular ejection fraction, high-voltage lead impedance and medications were gathered to determine what effect these variables had on the DFT levels. Of the 34 patients who had undergone waveform adjustment (group A), 27 (79%) were found to have satisfactory DFTs, while 41 (58%) of the 71 patients with fixed-tilt devices (group B) had satisfactory DFTs. Waveform duration adjustment was found to significantly increase the proportion of patients with satisfactory DFTs (p = 0.03)., (Copyright © 2013 S. Karger AG, Basel.)

A 65 year-old woman developed tachycardia and hypotension during haemodialysis. The non-contact mapping system was used to localise the origin of focal atrial tachycardia, and showed a remote from the endocardium focus. We discuss techniques that are helpful in identifying the origin, the area of preferential conduction, and the endocardial breakthrough of tachycardia.

We present a patient at risk of sudden cardiac death in whom ventricular fibrillation was effectively treated by wearable automatic defibrillator. We discuss the technical aspects of the device, current indications for this therapy and outcomes.

The implantable cardioverter defibrillator (ICD) has become the primary therapy for the treatment of potentially lethal ventricular arrhythmias. Ventricular arrhythmias encompass a spectrum of rhythm disturbances ranging from the occasional monomorphic ventricular premature complex to the almost universally fatal ventricular fibrillation. Our understanding of the mechanisms of ventricular fibrillation and defibrillation is still in evolution. At present, the most common ICD configuration consists of a pectoral pulse generator (active-can) with a bipolar transvenous dual coil lead. A transvenous system with an active-can has improved defibrillation thresholds and the ease of implantation. However, there are various clinical scenarios in which patients with high defibrillation threshold (DFT) are encountered. Although the incidence of high DFT patients is low, it is of significant concern since it may account for sudden cardiac death in patients with ICDs. At present, there are few clinical trials that are rigorous and well designed, and which can define a perfect methodology for the treatment of high DFT patients. In this review, in the context of commonly encountered clinical scenarios, we discuss therapeutic strategies to help manage patients with high DFT.

To map changes in neuronal activity in the brains of Dahl salt-sensitive (Dahl S) vs. salt-resistant (Dahl R) rats by high-sodium diet, we used immunohistochemical detection of Fra-like proteins as a marker for long-term neuronal activation. Compared with Dahl R rats during regular sodium intake, Dahl S rats showed modestly higher expression of Fra-like immunoreactivity (Fra-LI) in the supraoptic nucleus, anterior hypothalamic area (AHA), central gray, and nucleus of solitary tract (NTS) at 5,6, and 9 wk of age but clearly elevated Fra-LI in the magnocellular part of the paraventricular nucleus (PVN) at 6 wk of age (but not at 5 and 9 wk). In the median preoptic nucleus (MnPO) Fra-LI was lower at 9 wk of age and no differences were observed in the parvocellular PVN and subfornical organ in Dahl S vs. Dahl R rats on regular sodium intake. Compared with Dahl S rats on a regular-sodium diet, Dahl S rats on a high-sodium diet from 4 to 9 wk of age had significantly increased blood pressure and experienced transient activation of magnocellular PVN and MnPO and virtually no changes in the activity of the parvocellular PVN, AHA, and NTS. In contrast, Dahl R rats showed marked activation in the magnocellular PVN after 1 and 2 wk on a high-sodium diet compared with Dahl R rats on a regular-sodium diet. The present study demonstrates that Dahl S rats show differential activation of brain areas participating in regulation of osmotic and cardiovascular homeostasis during development of sodium-sensitive hypertension.

The role of endogenous centrally released nitric oxide (NO) during hypovolemia was investigated in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Bleeding of the rats (1.3% of blood volume) was performed after intracerebroventricular (ICV) administration of: 1) artificial cerebrospinal fluid (series 1, time control, 8 WKY and 8 SHR); 2) 0.5 mg NG-nitro-L-arginine (L-NNA, 2.3 nmol), an inhibitor of NO synthesis (series 2, 8 WKY and 7 SHR); and 3) 0.5 mg L-NNA followed by 1 mg (5.8 nmol) of L-arginine (L-Arg) (6 WKY and 5 SHR). In WKY, hypotension was associated with significant bradycardia (P < 0.001), whereas in SHR slight acceleration of heart rate was observed. In series 2 hemorrhage resulted in a small but significant increase of mean arterial pressure (MAP; P < 0.05) and considerable tachycardia (P < 0.001). In SHR, L-NNA did not modify the decrease of MAP during hypovolomia, and bleeding resulted in a significant bradycardia (P < 0.001). Pretreatment with L-Arg in series 3 was able to reverse the effects of L-NNA on changes of MAP and heart rate during hypovolemia. The results indicate that the central nitroxidergic system plays a significant role in eliciting hypotension and bradycardia in normotensive WKY during hemorrhage. Function of the central nitroxidergic system is significantly altered in SHR in which NO appears to prevent hemorrhagic bradycardia and to reduce the hypotensive effect.

The present study was designed to determine the role of centrally released arginine vasopressin (AVP) in cardiovascular adaptation to hypotensive hypovolemia in conscious normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Three groups of experiments were performed on WKY and SHR chronically implanted with lateral cerebral ventricle (LCV) cannulas and with femoral artery catheters. Mean arterial pressure (MAP) and heart rate (HR) were monitored before and after arterial bleeding (1.3% body weight) performed during LCV infusion 1) artificial cerebrospinal fluid (control), 2) V1 AVP-receptor antagonists {[d(Et2)Tyr(Me)]DAVP, 5 ng/min}, and 3) V2 AVP-receptor antagonists {[d(CH2)5-D-Ile2, Ile4, AlaNH2]AVP, 5 ng/min}. In control experiments hemorrhage caused similar significant decreases of MAP in both strains and bradycardia in WKY. Blockade of central V1 AVP receptors abolished hemorrhagic bradycardia and significantly reduced hypotension in WKY, with no effect on HR and MAP responses to hypovolemia in SHR. Neither in WKY nor in SHR were the cardiovascular responses to hemorrhage altered by blockade of central V2 receptors. The results suggest that the central V1 AVP system plays a significant role in eliciting hypovolemic bradycardia and hypotension in WKY and that this function is significantly impaired in SHR.