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We present a case of a 21-year-old female with congenitally corrected transposition of the great vessels and episodes of supraventricular tachycardia. We performed an electrophysiological study and successful ablation using an electro-anatomical mapping system. A single His bundle appeared to be located at the apex of the triangle of Koch and at electrophysiological study there was evidence of triple antegrade AV nodal pathways--slow, intermediate and fast, with two types of AV nodal re-entrant tachycardias. A series of radiofrequency ablations in the right posteroseptal area eliminated both slow and intermediate pathway conduction and cured the tachycardias.

Effective treatment of recurrent drug-refractory ventricular tachycardia is difficult, and conventional pharmacological and interventional approaches are often ineffective. We present a novel case report illustrating the potential use of omega-3 fatty acid supplementation in such patients.

Background: Atrial fibrillation (AF) is frequently initiated by focal activity originating in the pulmonary veins. We present the early and long-term results of a focal approach to pulmonary-vein ablation for cure of paroxysmal AF., Aims: The aim of this study was to establish the effectiveness of focal pulmonary vein radiofrequency ablation (RFA) for cure of paroxysmal AF., Methods: Fifty-one consecutive patients (35 male; 45+/-11.4 years) were considered for RFA on the following criteria: (i) symptomatic drug refractory AF, (ii) high-density atrial ectopy, bursts of atrial tachycardia or AF, (iii) absence of structural heart disease and (iv) provision of informed consent. Pulmonary vein mapping and RFA were by single trans-septal puncture, which was only performed in patients with adequate focal activity at the time of procedure. Focal activity was present spontaneously or was elicited by isoprenaline, burst pacing or AF induction and cardioversion., Results: One patient was excluded from the analysis due to non-pulmonary vein triggers. Trans-septal mapping and RFA were not performed in 22 patients (44%) due to: (i) inadequate ectopy (17), (ii) recurrent AF (1), (iii) inability to cross septum (2) and (iv) multiple foci (2). Of 28 patients, RFA was attempted with procedural success in 23 patients (82%), with no acute complications. Mean fluoroscopy time for patients having RFA was 29+/-11.5 mins. Pulmonary vein stenosis occurred in one case. Ten patients had symptomatic recurrence and, of those, two had further RFA. At a mean follow up of 11+/-8 months, 15 patients (54% ablated, 30% of the total cohort) remained free of AF without antiarrhythmics., Conclusion: This series highlights the low long-term success rate of RFA to cure AF by targeting pulmonary vein initiators using a focal approach. Electrical pulmonary vein isolation may provide better long-term results.

Introduction: Catheterization of the coronary sinus (CS) from the femoral vein can be challenging. We tested whether use of a long preshaped sheath facilitates CS cannulation., Methods and Results: One hundred four patients were randomized into two phases. In phase 1, consecutive patients were allocated to CS catheterization using the long sheath (n = 26) or standard 7-French 15-cm sheath (n = 25). If unsuccessful within 10 minutes, the alternative technique was used. Phase 2 assessed the utility of the long sheath in difficult cases. All patients initially were approached using the standard sheath. If cannulation failed after 10 minutes, patients were randomly allocated to the standard or long sheath approach. In phase 1, the standard approach failed in 4 (16%) of 25 cases. In each case, a long sheath proved successful (mean 3.2 min). The long sheath approach was successful within 10 minutes in all 26 cases. Catheter deployment was significantly quicker with the long sheath, but this was offset by the time required for sheath insertion. In phase 2, the standard approach was successful in 46 (87%) of 53 cases. Of 7 "failures," 3 were randomized to continue the standard approach, which was successful in 1; 4 were randomized to the long sheath approach, and success was achieved in all (mean 4.4+/-1.5 min). Overall, the CS could not be promptly catheterized in 15% of cases within 10 minutes using the standard sheath, and no failures were seen using the long sheath. No complications arose from the use of either technique., Conclusion: The long sheath was uniformly successful in permitting catheterization of the CS from the femoral approach in both unselected and difficult cases.

Aims: Resting plasma levels of atrial natriuretic peptide and B-type natriuretic peptide rise with left ventricular dysfunction, but little is known about effects of cardiac ischaemia on atrial natriuretic peptide and B-type natriuretic peptide levels during exercise. We investigated exercise levels of atrial natriuretic peptide and B-type natriuretic peptide in patients with suspected angina to determine whether these measurements could improve non-invasive assessment of coronary disease severity., Methods and Results: One hundred patients performed an exercise test (Bruce protocol) within 2 weeks of coronary angiography. Plasma levels of atrial natriuretic peptide and B-type natriuretic peptide were measured at rest and at peak exercise. Multivariate regression analysis was used to assess effects of age, sex, coronary anatomy, exercise time and ventricular function on atrial natriuretic peptide and B-type natriuretic peptide levels. Increasing age and female sex were significantly associated with higher resting atrial natriuretic peptide levels; age alone was associated with higher exercise atrial natriuretic peptide levels. As expected, left ventricular end-diastolic pressure and disease of left anterior descending and circumflex coronary arteries were associated with increased resting B-type natriuretic peptide levels. However, the usual rise in B-type natriuretic peptide levels during exercise was independently reduced by disease of the right coronary artery., Conclusion: This paradoxical effect of right coronary artery disease limits the value of natriuretic peptide measurements as predictors of coronary disease severity. Impaired release of B-type natriuretic peptide may reduce exercise tolerance in patients with right coronary artery disease.

Approximately 50% of the forearm vasodilatation to intra-arterial infusions of acetylcholine is mediated by endothelium-derived nitric oxide. These conclusions have been derived from venous occlusion plethysmographic measurements of total forearm blood flow during co-infusions of acetylcholine and NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide synthase. Since venous occlusion plethysmography measures total limb blood flow, the relative proportion of the measurement from skin cannot be determined precisely. To determine the effects of acetylcholine on skin specifically, we have used laser Doppler flowmetry to measure vascular responses to local iontophoresis of acetylcholine in the forearm of normal male volunteers. To elucidate the possible mechanisms of cutaneous vasodilatation to acetylcholine, vascular responses were measured before and after systemic inhibition of prostanoid production and nitric oxide synthesis by oral aspirin (600 mg daily for 3 days) and intravenous L-NMMA (3 mg/kg for 60 min), respectively. After aspirin administration, dose-dependent vascular responses to acetylcholine were reduced significantly by approximately 53% (p < 0.005, ANOVA). In contrast, intravenous L-NMMA appeared to have no significant effect on cutaneous vascular responses to acetylcholine. While the role of nitric oxide is uncertain, vasodilatation to acetylcholine in the forearm skin is mediated largely by a prostanoid-dependent mechanism. Assessment of cutaneous vascular responses to iontophoresis of acetylcholine may, therefore, be useful in diseases where abnormal endothelium-dependent prostanoid function has been implicated.

Although elevations of plasma atrial natriuretic peptide (ANP) concentrations have been shown to have prognostic significance in patients after acute myocardial infarction (AMI), the relation between plasma levels of B-type natriuretic peptide (BNP) and cardiovascular mortality remains unknown. To test the prognostic value of plasma ANP and BNP after AMI, plasma concentrations were measured a mean of 3 days after infarction in 75 patients. During a median follow-up of 19.7 months, 14 patients (18.4%) died of cardiovascular causes. On univariate analysis, plasma ANP and BNP, Killip class, modified Peel index, left ventricular ejection fraction, and presence of left ventricular failure were all associated with cardiovascular mortality. In contrast, plasma ANP was the only variable that correlated with the development of symptomatic heart failure and hospitalization. For the combined end point of cardiovascular mortality, symptomatic heart failure, and hospitalization, plasma neurohormones were the only variables of predictive value. By stepwise regression analysis, plasma BNP was the only significant independent predictor of cardiovascular mortality (p = 0.001), whereas plasma ANP identified patients at risk of symptomatic heart failure and hospitalization (p = 0.002 and 0.019, respectively). This study indicates that plasma BNP measured after AMI is a powerful neurohormonal predictor of subsequent cardiovascular mortality, whereas plasma ANP correlates better with the development of symptomatic heart failure and hospitalization. Routine measurement of both of these peptides in the period immediately after an AMI may provide a simple means of risk stratification with different information gained from each peptide.

Objective: To assess the differential effects of low dose (5 mg) and high dose (20 mg) lisinopril treatment on cardiovascular hormones, renal function, and blood pressure over 24 hours in patients with heart failure., Design: Double-blind crossover study., Setting: Department of Clinical Pharmacology, Ninewells Hospital and Medical School, Dundee., Patients: 19 patients with chronic heart failure and left ventricular ejection fraction < or = 45%., Results: Plasma concentrations of aldosterone and endothelin were lower on the 20 mg dose (plasma aldosterone mean at peak drug effect: 90.7 v 152.0 pg/ml, P < 0.001; mean at trough effect: 124.7 v 174.4 pg/ml, P < 0.01; plasma endothelin at trough effect 4.70 v 6.04 pmol/l, P = 0.03). Creatinine clearance was lower on 20 mg lisinopril (68.7 v 82.1 ml/min, P < 0.05). The area under the curve for diastolic blood pressure over 24 hours was significantly lower on 20 mg (mean difference 3.0 mm Hg, P = 0.04); for systolic blood pressure there was a similar trend (mean difference 5.7 mmHg, P = 0.05). Plasma concentrations of atrial natriuretic peptide (ANP) and B-type natriuretic peptide were similar for both doses; urinary excretion of ANP was lower on 20 mg (12.2 v 13.6 pmol, P < 0.05)., Conclusions: These results indicate that within the usual therapeutic range, high doses of lisinopril cause greater suppression of selected cardiovascular hormones than low doses in heart failure, but are associated with lower creatinine clearance in some patients.

We have directly compared atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and N-terminal pro-ANP (N-ANP) as markers of patients with left ventricular ejection fraction (LVEF) < or = 35%, as measured by radionuclide ventriculography. Venous blood samples were obtained from an unselected group of 87 patients who had been referred for assessment of ventricular function. ANP, BNP, and N-ANP were measured by radioimmunoassay using commercial kits. Receiver-operating characteristic analysis was used for the objective assessment of the diagnostic performance of each assay. There was a weak negative correlation between LVEF and plasma levels of ANP-li (r = -0.50,), BNP-li (r = -0.57), and N-ANP-li (r = -0.49) (p <0.01 for each peptide). Areas under the receiver-operating characteristic curves for BNP (0.880) and N-ANP (0.832) were not significantly different from each other, but were both significantly greater than the value for ANP (0.761): BNP versus ANP, p <0.01; and N-ANP versus ANP, p <0.05. The optimal sensitivity and specificity of each assay for the detection of patients with LVEF < or = 35% were: BNP > 4 pmol/L-sensitivity 1.0, specificity 0.58; N-ANP >200 pmol/L-sensitivity 0.95, specificity 0.35; and ANP >10 pmol/L-sensitivity 0.90, specificity 0.30. Plasma concentrations of BNP and N-ANP provide sensitive indicators of moderate to severe LV dysfunction; both peptides, are objectively superior to ANP for identifying patients with LVEF < or = 35%. These simple tests could be used to screen patients with suspected ventricular dysfunction to reduce the demand for further cardiac investigations.

Background: Atrial and B-type natriuretic peptide are both known to be antagonists of the renin-angiotensin system. C-type natriuretic peptide (CNP) is a new member of this family except that its principal source is the vascular endothelium. This study tested the hypothesis that CNP is a local inhibitor of vascular angiotensin-converting enzyme (ACE) activity., Methods and Results: Vascular ACE activity was assessed by the differential vascular response to angiotensin I and angiotensin II. Healthy male volunteers were studied with the use of brachial artery infusions of angiotensin I and angiotensin II at two doses, with and without coinfusion of CNP at 500 pmol/min (n=8) and hydralazine at 10 microgram/min (n=8) (as a nonspecific vasodilator control). CNP alone and hydralazine alone caused similar increases in forearm blood flow (CNP+, 93.0+/-14.8%; hydralazine+, 84.2+/-22.6%). CNP inhibited the vasoconstrictive effect of angiotensin I (reduction in overall effect with CNP, 56.8+/-12.9%, P<.001) but not that of angiotensin II. Hydralazine did not significantly inhibit the effect of either angiotensin I or angiotensin II., Conclusions: This evidence of a differential effect of CNP on the vascular response to angiotensin I but not to angiotensin II suggest that CNP acts as a local endogenous regulator of vascular ACE activity in the human forearm resistance vessels.