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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).

Cardiac perforation due to a pacemaker or defibrillator lead occurs at a rate of 0.4–2.0%. Since first described [1], the overall incidence has decreased significantly. The reported incidence of this complication has been as low as < 1 % to as high as 15% [2-4]. Of 4,280 permanent pacemaker (PPM) implants only 50 (1.2%) patients developed a significant effusion and symptoms consistent with a perforation [5]. The incidence of this complication from the time of surgery decreases over time. By convention, a perforation detected within 24 hours, is classified as acute. If detected within 30 days of implantation (usually 5 days4 weeks), it is referred to as early (sub-acute); and, those detected after 30 days referred to as late, delayed or chronic perforation. The majority of perforations manifest within a year but rarely cases have been reported as late as five years following implantation. [6]

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.

The purpose of the present study was to compare influence of central arginine vasopressin (AVP) and of atrial natriuretic peptide (ANP) on control of arterial blood pressure (MAP) and heart rate (HR) in normotensive (WKY) and spontaneously hypertensive (SHR) rats. Three series of experiments were performed on 30 WKY and 30 SHR, chronically instrumented with guide tubes in the lateral ventricle (LV) and arterial and venous catheters. MAP and HR were monitored before and after i.v. injections of either vehicle or 1, 10 and 50 ng of AVP and 25, 125 and 500 ng of ANP. Sensitivity of cardiac component of baroreflex (CCB), expressed as a slope of the regression line was determined from relationships between systolic arterial pressure (SAP) and HR period (HRp) during phenylephrine (Phe)-induced hypertension and sodium nitroprusside (SN)-induced hypotension. CCB was measured before and after administration of either vehicle, AVP, ANP, or both peptides together. Increases of MAP occurred after LV administration of 1, 10 and 50 ng of AVP in WKY and of 10 and 50 ng in SHR. ANP did not cause significant changes in MAP in both strains as compared to vehicle, but it abolished AVP-induced MAP increase in WKY and SHR. CCB was reduced in WKY and SHR after LV administration of AVP during SN-induced hypotension. In SHR but not in WKY administration of ANP, AVP and ANP + AVP decreased CCB during Phe-induced MAP elevation. The results indicate that centrally applied AVP and ANP exert differential effects on blood pressure and baroreflex control of heart rate in WKY and SHR and suggest interaction of these two peptides in blood pressure regulation at the level of central nervous system.

nosis of GERD increases the relative risk of AF by 39%, before correction, and by 8–19% after correction for known AF risk factors as well as for coronary artery dis-ease [8]. V arious mechanisms have been postulated to ac-count for an association between GERD and AF. The foremost is the common denominator – inflammation. GERD is associated with local inflammation in the gas-trointestinal tract induced by

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.

We describe a rare case of Twiddler's syndrome that resulted in a complex ICD lead fracture involving both the insulation and the conductor. The conductor fracture resulted in noise artefact that was interpreted by the device as ventricular fibrillation, but the patient had not received any shocks because the "episodes" were non-sustained. The patient did not have traditional risk factors for Twiddler's syndrome.

Congenital long QT syndrome is an inherited disorder of cardiac repolarization that predisposes to syncope and to sudden death from polymorphic ventricular tachycardia. The disorder should be suspected when the electrocardiogram shows characteristic QT abnormalities, or when there is a family history of long QT syndrome or of an event that raises suspicion of long QT syndrome, such as sudden death, syncope, or ill-defined "seizure" disorder. We can now classify some types of congenital long QT syndrome according to their genetic mutations and their triggers, such as exercise, rest, or startle.

[8, 9] . Although it carried a high success rate, the com-plexity of the technique and significant prolongation of cardiopulmonary bypass time made it unattractive dur-ing mitral valve repair. The development of a variety of ablative energy sources now allows creating a similar set of lesions without excessive prolongation of the proce-dure. In this issue of

Pressor responses to increases in cerebrospinal fluid (CSF) sodium in Wistar rats and to high salt intake in spontaneously hypertensive rats (SHR) involve both brain ouabainlike activity (“ouabain”) and the brain renin-angiotensin system (RAS). Because some of the effects of “ouabain” are mediated by the median preoptic nucleus (MnPO) and this nucleus contains all elements of the RAS, the present study assessed possible interactions of “ouabain” and ANG II in this nucleus. In conscious Wistar rats, injection of ANG II into the MnPO significantly increased mean arterial pressure (MAP) and heart rate (HR). This response was not affected by pretreatment with a subpressor dose of ouabain. MAP and HR increases by ouabain in the MnPO were significantly attenuated by MnPO pretreatment with losartan. In Wistar rats, losartan in the MnPO also abolished pressor and HR responses to intracerebroventricular 0.3 M NaCl and attenuated MAP and HR responses to intracerebroventricular ouabain. Five weeks of a high-salt diet in SHRs resulted in exacerbation of hypertension and increased responses to air-jet stress and intracerebroventricular guanabenz. Losartan injected into the MnPO reversed the salt-sensitive component of the hypertension and normalized the depressor response to guanabenz but did not change responses to air-jet stress. We conclude that in the MnPO, ANG II via AT1 receptors mediates cardiovascular responses to an acute increase in CSF sodium as well as the chronic pressor responses to high sodium intake in SHR.

The functional role of the vascular endothelium is a subject of growing interest and appreciation. Some of the key functions of the endothelium are modulated by the activity and expression of endothelial nitric oxide synthase (eNOS), suggesting a role for this enzyme in endothelial dysfunction. Several well-known angiogenic stimulators exert their effect only in the presence of the functional eNOS. In this setting NO production is responsible for the scalar podokinetic cell motility, which is a prerequisite for the acquisition of vectorial movement when guidance cues are applied. The mode of this NO action appears to lie in the accelerated turnover of focal adhesions through the process of activation/inactivation of protein tyrosine phosphatases. Localization of eNOS to the caveolar domains, in the proximity of clustered beta1 integrins, provides an additional level of regulatory complexity through the modulation of caveolar dynamics and the state of caveolin oligomerization. Therefore, eNOS serves various important functions in the endothelium and is a putative target for therapeutic interventions.

1. Among the diverse functions of endothelins (ET), their role in the remodelling of blood vessels remains poorly examined. In the present review, we summarize findings obtained in our laboratory and present four independent lines of evidence to support this novel function. We also demonstrate that the motogenic and angiogenic effects of ET are mediated via the ETB receptor and that the functional endothelial nitric oxide synthase (NOS) is requisite for this action. 2. We demonstrated that ET stimulates transmigration of endothelial cells in a modified Boyden chamber and accelerates endothelial wound healing acting via ETB receptors. 3. In genetically engineered Chinese hamster ovary cells expressing either ETB receptor or endothelial NOS or both, application of ET results in accelerated cell migration only when the receptor and the enzyme are coexpressed. Application of antisense oligonucleotides producing a specific knockdown of the endothelial NOS results in the loss of ET ability to stimulate endothelial cell migration in response to ET. 4. Finally, using a novel model of in vivo angiogenesis, we were able to demonstrate that ET enhances formation of new vessels, but this effect requires functional endothelial NOS. 5. The described phenomenon of NO production, serving as a prerequisite for endothelial cell locomotion in response to activation of ETB receptor may explain a host of pathophysiological observations on inadequate angiogenesis despite enhanced generation of ET-1. 6. Based on the contribution of endothelial cell migration to angiogenesis, these data may implicate insufficient NO production in pathological states (e.g. atherosclerosis, heart failure and hypertension) in the inappropriate response to angiogenic stimuli.

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 inverted question mark[d(Et2)Tyr(Me)]DAVP, 5 ng/min inverted question mark, and 3) V2 AVP-receptor antagonists inverted question mark[d(CH2)5-D-Ile2, Ile4, AlaNH2]AVP, 5 ng/min inverted question mark. 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.

The effects of arginine vasopressin analogs with V2 agonistic and antagonistic properties on blood pressure (BP) and heart rate (HR) were compared in conscious, spontaneously hypertensive (SHR) and normotensive (WKY) rats under resting conditions and after administration of phenylephrine (Phe) and sodium nitroprusside (SN). In WKY rats, resting BP and HR were not significantly affected during intravenous (i.v.) infusion of dVDAVP, (V2 agonist; 200 pg/kg/min), d(CH2)5 (D-Ile2,Abu4]AVP (V2 antagonist 1; weak V1 antagonist; V2/V1 ratio = 29; 0.6 microgram/kg/min), d(CH2)5[D-Ile2,Ile4,AlaNH2]AVP (V2 antagonist 2; very weak V1 antagonist; V2/V1 ratio = 83; 0.6 microgram/kg/min) and combined infusion of V2 agonist and V2 antagonist 2. Under resting conditions BP and HR were not affected in WKY by any of the treatments. In SHR rats BP and HR were significantly decreased by V2 antagonist 2 infused alone or in combination with V2 agonist. In WKY but not in SHR V2 agonist without and with prior V2 receptors blockade significantly augmented bradycardia associated with a maximum increase of the systolic blood pressure after Phe administration. Significant differences were found between SHR and WKY in SN-induced changes of HR and BP after administration of V2 agonist and antagonists. The results suggest that circulating vasopressin may modify the baroreflex by interaction with receptors which are stimulated by V2 agonist but are different from the classical V2 receptors. The study supports evidence for differential effects of vasopressin analogs on blood pressure and blood pressure-heart rate relations in WKY and SHR.

Blood pressure and heart rate responses to intracerebroventricular (ICV) injections of atrial natriuretic peptide (ANP, 125 ng) arginine vasopressin (AVP, 10 ng), combination of ANP (125 ng) and AVP (10 ng) or artificial cerebrospinal fluid (acsf, 5 microliters) were compared in conscious normotensive (WKY) and spontaneously hypertensive (SHR) rats. In both strains, ICV injection of AVP elicited significant increase of mean blood pressure (MP) and heart rate (HR). Increase of MP but not of HR was significantly greater in SHR than in WKY (p less than 0.05). Injection of acsf or ANP, as well as simultaneous administration of ANP and AVP, did not elicit significant changes of MP either in WKY or in SHR. In SHR, HR was significantly elevated by ICV injections of AVP and ANP + AVP, whereas in WKY HR was increased only after AVP. The data suggest that interaction of ANP and AVP at a central level may result in significant attenuation of central pressor effects of vasopressin.

The influence of naloxone on recovery from hemorrhagic hypotension was investigated in conscious normotensive and spontaneously hypertensive (SHR) Wistar-Kyoto rats. In both groups arterial blood pressure (MBP) was reduced to 50% of the resting level by arterial bleeding. Administration of naloxone (0.02 mg/kg iv) significantly impaired restitution of MBP in WKY and SHR in comparison to control experiments on WKY and SHR receiving no naloxone. The magnitude of this effect was similar in both strains, however in SHR, it appeared with a significant delay. The results indicate that small doses of naloxone may suppress recovery from hemorrhagic hypovolemia.

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.