Leadless AV pacemaker after RF ablation for treatment of bundle branch reentrant ventricular tachycardia: A case report.

In the present article we report the case of a patient at high risk of infection wearing a subcutaneous ICD (S-ICD) due to previous system extractions, hospitalized for symptomatic BBR VT and underwent radiofrequency catheter (RF) ablation. Afterwards, to prevent the possible progression of the infra-His conduction disease to a complete block, it was decided to implant a pacemaker system. Since the high infectious risk, and the patient's firm refusal to implant another transvenous system given the previous extractions he underwent in the past, it was decided to implant a leadless pacemaker with atrioventricular synchrony.

Vascular dysfunction after repair of coarctation of the aorta: impact of early surgery.

BACKGROUND: Patients with repaired coarctation are at increased risk of hypertension and cardiovascular disease despite successful repair. We studied the function of conduit arteries in upper and lower limbs of patients late after successful coarctation repair and its relation to age at surgery. METHODS AND RESULTS: Flow-mediated dilatation (FMD) and the dilatation after sublingual nitroglycerin (NTG, 25 microgram) were measured by using high-resolution ultrasound in the brachial artery in 64 coarctation patients (44 males and 20 females, aged 19+/-10 years; median age at operation 4 months) and 45 control subjects (28 males and 17 females, aged 19+/-10 years) and in the posterior tibial artery in 37 patients and 22 control subjects. Arterial stiffness was determined by pulse-wave velocity (PWV) of the brachioradial and femoral-dorsalis pedis tracts. Patients, compared with control subjects, had lower brachial FMD (7.16+/-3.4% versus 8.62+/-2.3%, respectively; P=0.02) and NTG (11.46+/-4.3% versus 13.21+/-4.6%, respectively; P=0.046) and higher brachioradial PWV (9.17+/-3.1 versus 8.06+/-1.9 m/s, respectively; P=0.05). In contrast, posterior tibial FMD, NTG, and lower limb PWV were comparable. Age (months) at the time of repair was related to brachioradial PWV (r=0.42, P=0.002) but not to brachial FMD or NTG. CONCLUSIONS: Patients with repaired aortic coarctation have impaired conduit artery function, with abnormal responses to flow and NTG, and increased vascular stiffness confined to the upper part of the body. Early repair is associated with preserved elastic properties of conduit arteries, but reduced reactivity remains.

Is insulin action a determinant of left ventricular relaxation in uncomplicated essential hypertension?

OBJECTIVE: To examine the relation of insulin action and left ventricular diastolic function in uncomplicated essential hypertension. METHODS: Doppler echocardiography and glucose clamping combined with indirect calorimetry were performed in 29, newly diagnosed, hypertensive men, free from cardiac and metabolic drugs. They were divided into two groups according to the clamp-derived whole-body glucose disposal level: 20 with insulin resistance (whole-body glucose disposal < 33 mumol/kg per min) and nine with normal insulin sensitivity. RESULTS: The two groups were comparable in age, body mass index, heart rate and blood pressure. No difference in diastolic function was found except for the isovolumic relaxation time, which was prolonged for patients with insulin resistance (P = 0.02). For the population as a whole, the relaxation time had univariate relations with the left ventricular mass index (r = 0.57, P < 0.001), whole-body glucose disposal (r = -0.56, P < 0.001) and non-oxidative glucose metabolism (r = -0.54, P = 0.002). In a multivariate model including age, body mass index, heart rate, diastolic blood pressure, left ventricular mass index and whole-body glucose disposal as potential determinants, only the left ventricular mass index (beta = 0.39, P = 0.02) and whole-body glucose disposal (beta = -0.38, P = 0.03) were independent predictors of the relaxation time (R2 = 0.43, P < 0.001). CONCLUSIONS: In uncomplicated essential hypertension the insulin resistance is a determinant of abnormalities in isovolumic relaxation, independently from the influence exerted by increased blood pressure levels, being overweight and left ventricular hypertrophy.

Impact of heart rate and atrioventricular delay on left ventricular diastolic filling in patients with dual-chamber pacing for sick sinus syndrome or atrioventricular block.

We examined the effect of left ventricular filling on different combinations of programmable heart rate and atrioventricular delay in patients with dual-chamber pacemakers. Pacing mode with heart rates of 60 beats/min and 156 ms of atrioventricular delay induced a diastolic pattern that resembles more than others the one observed in healthy subjects in sinus rhythm.

Effects of short-term reduction in serum cholesterol with simvastatin in patients with stable angina pectoris and mild to moderate hypercholesterolemia.

To evaluate the effects of short-term cholesterol-lowering treatment on myocardial effort ischemia, 22 patients with stable effort ischemia and mild to moderate hypercholesterolemia (low density lipoprotein [LDL] cholesterol 160 to 220 mg/dl) were randomly allocated at baseline (TO) in 2 groups. Group A included 12 patients treated with simvastatin 10 mg bid; group B included 10 patients treated with placebo. All patients underwent a treadmill electrocardiography (ECG) test; total cholesterol, HDL and LDL cholesterol, triglycerides, plasma, and blood viscosity were measured. All tests were repeated after 4 and 12 weeks. For 18 of the same patients (11 taking simvastatin, 7 receiving placebo), forearm strain-gouge plethysmography was performed at baseline and after 4 weeks, both at rest and during reactive hyperemia. At 4 and 12 weeks, group A showed a significant reduction in total cholesterol (p <0.05) and LDL (p <0.05), with unchanged HDL, triglycerides, blood, and plasma viscosity. Effort was unmodified, ST-segment depression at peak effort and ischemic threshold were significantly improved after 4 and 12 weeks (all p <0.05) with unchanged heart rate x systolic blood pressure product. A significant increase in the excess flow response to reactive hyperemia was detected in group A (p <0.03); group B showed no changes in hematochemical and ergometric parameters. These data suggest that cholesterol-lowering treatment is associated with an improvement in myocardial effort ischemia; this might be explained by a more pronounced increase of coronary blood flow and capacity of vasodilation in response to effort.

Right atrial appendage thrombosis in atrial fibrillation: its frequency and its clinical predictors.

This study assesses the incidence of right atrial (RA) chamber and appendage thrombosis in patients with atrial fibrillation (AF) in relation to RA appendage morphology and function. Transthoracic and multiplane transesophageal echocardiography were performed in 102 patients with AF to assess the incidence of RA and left atrial (LA) thrombi and spontaneous echo contrast. Both right and left ventricular sizes, atrial chamber and appendage sizes and function were measured. Twenty-two patients in sinus rhythm served as the control group (SR). Complete visualization of the RA appendage was feasible in 90 patients with AF. Patients with AF had lower tricuspid annular excursion (p = 0.008) and larger RA chamber area (p = 0.0001) than patients in SR. In addition, RA appendage areas were larger (p <0.05) and RA ejection fraction and peak emptying velocities (both p <0.0001) were lower in patients with AF patients than in those in SR. Equivalent differences were found for the LA appendage. Six thrombi were found in the RA appendage and 11 thrombi in the LA appendage in AF patients. Spontaneous echo contrast was found in 57% and 66% in the right atrium and in the left atrium, respectively. AF patients with RA appendage thrombi had a larger RA area (p = 0.0001), and lower RA appendage ejection fraction and emptying velocities (both p = 0.0001) than patients without thrombi. Spontaneous echo contrast was detected in all patients with thrombi. Spontaneous echo contrast was the only independent predictor of RA (p = 0.03) and LA appendage thrombosis (p = 0.036). In conclusion, multiplane transesophageal echocardiography allows the assessment of RA appendage morphology and function. RA spontaneous echo contrast is the only independent predictor of RA appendage thrombosis.

Favourable interaction of calcium antagonist plus ACE inhibitor on cardiac haemodynamics in treating hypertension: rest and effort evaluation.

The aim of the study was to evaluate the effects of verapamil sustained release (SR) 240 mg, enalapril and their combination on blood pressure (BP) and cardiac haemodynamics at rest and during exercise in 20 patients with moderate essential hypertension (seven men and 13 women, mean age +/- s.d. 53.7 +/- 15.8 years). After a 4 week placebo run-in period, patients were randomly allocated to received verapamil SR 240 mg once daily or enalapril 20 mg once daily for 4 weeks in a double-blind fashion. Patients whose diastolic blood pressure (DBP) was still > or = 95 mm Hg at the end of this period received verapamil SR plus enalapril for an additional 4 weeks. At the end of the placebo, single and combined treatment periods, resting and exercise (bicycle ergometry) haemodynamics were evaluated by radionuclide ventricular angiography (technetium-99m) and the following parameters were assessed: BP, heart rate, double product, systemic vascular resistances (SVR), cardiac output (CO), stroke volume (SV), ejection fraction (EF) mean ejection rate (mER) and peak filling rate (PFR). Both verapamil SR and enalapril monotherapies significantly reduced resting and exercise BP (P < 0.01), with a BP normalisation (DBP < or = 95 mm Hg) of five of 10 and 4 of 10 patients respectively. A greater BP fall and a normalisation of 11 of 11 patients was obtained in non-responders to monotherapy, when treated with verapamil SR and enalapril (P < 0.01). Verapamil SR also reduced heart rate at rest and during exercise (-11.8% and -18.4%, respectively, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Electrophysiological analysis of atrioventricular and intraventricular conduction in bi- and tri-fascicular blocks]. / Analisi elettrofisiologica della conduzione atrioventricolare ed intraventricolare nei blocchi bi- e tri fascicolari.

We have evaluated, at baseline and during incremental atrial pacing (AP), intracardiac conduction features of 53 patients with electrocardiographic diagnosis of bifascicular or trifascicular block, free from any pharmacological treatment potentially able to affect atrioventricular (AV) conduction system properties. The patients have been subdivided in the following groups: group A (13 patients), with LBBB and a PQ interval > or = 200 msec; group B (14 patients), with RBBB, LAH with a PQ interval > or = 200 msec; group C (8 patients), with LBBB and a PQ < 200 msec; group D (15 patients), with RBBB, LAH and a PQ < 200 msec; group E (3 patients), with RBBB, LPH and a PQ < 200 msec. In group A, 31% presented a long AH interval (> 140 msec), while 85% showed an increased infra-his conduction time (HV > 55 msec). During AP, only 38.5% maintained a 1:1 AV conduction ratio up to 140 bpm, while 30.8% developed an infra-his Mobitz 2 2nd degree AV block. 15.4% an infrahis 2:1 2nd degree AV block, 15.4% an AV nodal Mobitz 2 2nd degree AV block. In group B, 64% and 29% exhibited respectively an AV nodal and an infrahis conduction delay. During AP, 57.1% maintained a 1:1 AV conduction ratio up to 140 bpm, 14.3% developed an AV nodal Mobitz 1 2nd degree AV block, 14.3% an infrahis Mobitz 1 2nd degree AV block, 7.1% an AV nodal 2:1 2nd degree AV block, 7.1% an infrahis Mobitz 2 2nd degree AV block. In group C, no patient manifested a prolonged AH interval, while 50% exhibited a HV > 55 msec. 62.5% maintained a 1:1 AV conduction ratio up to 140 bpm, 25% developed an AV nodal Mobitz 1 2nd degree AV block and 12.5% an infrahis 2:1 2nd degree AV block. In group D, no patient showed an increased AH interval and only 13% presented a HV interval exceeding 55 msec. During AP, 86.7% maintained a 1:1 AV conduction ratio up to 140 bpm, 6.6% developed an AV nodal Mobitz 1 2nd degree AV block, 6.6% an infrahis 2:1 2nd degree AV block. In group E, no patient showed a prolonged AH interval, while 2/3 (66.6%) exhibited an infrahis conduction delay. During AP, 100% developed an infrahis 2:1 2nd degree AV block. Considering all patients with LBBB (groups A+C) and with RBBB+LAH (groups B+D), no differences were found in terms of PQ, PA and AH intervals, even though, concerning patients with a long PQ (group A vs group B), AH interval resulted significantly longer in patients with RBBB+LAH (121.85 +/- 36.4 msec vs 163.29 +/- 55.96 msec, p = 0.031). Infrahis conduction, independently from the measurement adopted (HVI interval: from the beginning of the His to the onset of the ventricular electrogram recorded at the His region; HV2 interval: from the beginning of the His to the onset of the surface QRS), resulted more compromised in patients with LBBB than in patients with RBBB+LAH (HVI: 75.24 +/- 40.23 msec vs 50.79 +/- 25.16 msec, p = 0.011; HV2: 77.24 +/- 38.12 msec vs 53.92 +/- 29.3 msec, p = 0.015). Such a difference became even more significant when comparing the percentage of patients with a prolonged HV interval (average value > 55 msec) in the above mentioned groups: 71.4% in case of LBBB, 20.7% in case of RBBB+LAH (p < 0.001). Regarding intraventricular conduction (IV), no statistically significant differences were found. In patients with RBBB+LAH, IV was not related to infrahis conduction time and PQ interval appeared more related to AH (r = 0.838, p < 0.001) than to HV (PQ-HV1: r = 0.381, p = 0.041, PQ-HV2: r = 0.474, p = 0.009). Conversely, in patients with LBBB infrahis and IV conduction appeared linearly related (HVI-V: r = 0.416, p = 0.06; HV2-V: r = 0.445, p = 0.043). As for PQ interval, it resulted more closely related to infrahis conduction (PQ-HVI: r = 0.626, p = 0.002; PQ-HV2: r = 0.674, p < 0.001), than to AH (r = 0.533, p = 0.013). In conclusion, infrahis conduction resulted more impaired in patients with LBBB. In this group, differently from patients with RBBB+LAH, infrahis conduction seems to affect the degree of IV conduction delay. (ABST

Cholesterol-lowering and vascular reactivity in relation to coronary heart disease.

Despite the strong evidence that cholesterol-lowering treatment is effective in the primary and secondary prevention of coronary heart disease, there is a great discrepancy between the results relating to prognosis and the ability of this treatment to induce regression of coronary atheromatous plaques. Since hypercholesterolemia causes a dysfunction in vascular reactivity, improvement can also be ascribed to restoration of vascular relaxation capacity. This conclusion is supported by a wealth of clinical and experimental evidence.

An unusual procedure for the treatment of simultaneous pericardial and pleural effusions.

BACKGROUND: Symptomatic posterior pericardial effusion (PE) represents a diagnostic challenge since it is not easy to quantify by echocardiography. In addition, this type of effusion is normally treated by surgery because of the difficulty in drainage. CASE: A 59-year-old male presented a symptomatic circumferential PE following mitral valve substitution. Two days after a successful percutaneous subcostal pericardiocentesis, he reported severe dyspnea with hypotension and pulsus paradoxus. At chest X-rays, he showed a left pleural effusion; echocardiography, also performed from the left posterior axillary line, showed a large posterior PE and a large pleural effusion separated by a membrane. A needle was inserted at the fourth intercostal space 2 cm medially to the left posterior axillary line and advanced into the pleural and then into the pericardial cavity under echocardiographic guidance. Serous-hemorrhagic fluid was drained from the pericardial (800 cc) cavity and, after retraction, from the left pleural cavities (600 cc), with consequent hemodynamic improvement. CONCLUSION: Pleuro-pericardiocentesis may represent a valid alternative to surgery for the treatment of cardiac tamponade due to posterior pericardial effusions, in the peculiar situation characterized by the simultaneous presence of a left pleural effusion. This procedure should be performed by qualified physicians under echographic guidance.

A double-blind comparison of nicorandil and metoprolol in stable effort angina pectoris.

The antianginal activities of nicorandil, 10 and 20 mg bid, and metoprolol, 100 mg bid, were compared in patients with stable effort angina pectoris in a randomized, double-blind parallel group study lasting 7 weeks. Twenty patients were enrolled into the trial and 16 patients completed the study. To evaluate the anti-ischemic effects of the two drugs, a treadmill exercise test was performed after a 1-week placebo run-in period and 6 weeks of treatment. On the same occasions, weekly sublingual nitroglycerin consumption and the number of anginal attacks were also recorded in the patient's diary. The total duration of exercise increased significantly with both nicorandil, 10 and 20 mg, and metoprolol (p < 0.01). Similar improvements were observed in the time to onset of ischemia with both treatments (p < 0.01). The double product at maximal comparable workload (MAX 1) was reduced with the two drugs (p < 0.05 for nicorandil and p < 0.01 for metoprolol), while at the maximal exercise time (MAX 2) it was reduced with metoprolol (p < 0.01) and slightly but not significantly increased with both doses of nicorandil. Weekly sublingual nitroglycerin consumption and anginal attacks were also significantly reduced a similar manner by both treatments (p < 0.01). In conclusion, nicorandil, 10 and 20 mg bid, exerted an anti-ischemic effect comparable with that of metoprolol in patients with stable effort angina pectoris.

Management of the patient with left ventricular hypertrophy.

The management of left ventricular hypertrophy (LVH) presupposes that the patient is identified by echocardiography and is carefully evaluated for risk stratification, taking into consideration possible associated complications. The role of non-pharmacological treatment is limited, except in obese patients. Drug treatment, especially using calcium antagonists, angiotensin converting enzyme inhibitors and beta-blockers, has proved to be effective in reducing LVH. These drugs are also effective in controlling, if not reversing, the associated pathophysiological changes and complications, such as impaired systolic and diastolic function, and ventricular arrhythmias. There is, however, no evidence of any beneficial effect on myocardial ischaemia. The desirable goal is LVH regression, but it may not be achievable in over 50% of patients, and it is not possible to identify patients in whom regression is likely. Regression, or control of each sequelae, could prevent sudden death, the evolution of hypertensive heart disease leading to heart failure and, probably, myocardial infarction. Patients must be followed carefully during and, particularly, at the beginning of the antihypertensive therapy which has to be gradually introduced. At best, blood pressure must be reduced while avoiding hypotension. The strategy of antihypertensive treatment has to be reconsidered on the basis of the presence of LVH and could lead to decreased cardiovascular morbidity and mortality of patients with LVH.

Treatment of hypertension associated with stable angina pectoris: favourable interaction between new metoprolol formulation (OROS) and nifedipine.

This was a double-blind, within-patient, crossover study to evaluate the effects of a new formulation of metoprolol on blood pressure (BP) and myocardial ischemia. Twenty outpatients with mild to moderate essential arterial hypertension, chronic stable angina pectoris and positive exercise test, after a 2-week baseline placebo period, were randomized to receive long-acting metoprolol (OROS) 14/190 mg o.d., nifedipine SR 20 mg b.i.d. or their combination in a sequence of a 3 x 3 Latin square design. Two patients withdrew from the study (1 for adverse event during metoprolol and 1 for rise of BP during nifedipine). Nifedipine, metoprolol and their combination significantly reduced the weekly number of angina attacks and nitroglycerin consumption with respect to baseline. The total number of ischemic events (at 24-hour ECG monitoring) significantly decreased after each treatment with respect to baseline. Twenty-four hours mean systolic and diastolic BP were reduced by both nifedipine alone and metoprolol alone; the combination of the two drugs led to a further decrease in both systolic and diastolic BP. The duration of silent ischemic episodes was significantly reduced by nifedipine and combination but not by metoprolol. On the other hand 24 hours symptomatic attacks/patient were significantly reduced by beta-blocker and combination, but not by nifedipine. Metoprolol alone and administered with nifedipine caused a decrease, with respect to placebo baseline, in 24-hour mean heart rate (HR) and reduced the increase of HR and systolic BP at the onset of ST depression during symptomatic ischemic episodes. The effort time and time to ST = -1 mm at treadmill were significantly increased by treatment with nifedipine alone, with metoprolol alone and with their combination, but the combination was more effective than the individual therapies. ST depression at peak exercise was significantly reduced by each treatment. The slopes of correlations between the ST-segment variation and systolic BP, HR and rate-pressure product during exercise, significantly decreased after all treatments with respect to placebo baseline, more with the combination therapy than with nifedipine alone and metoprolol alone. In conclusion, based on our results the favourable interaction of metoprolol OROS and nifedipine given concomitantly, is likely to be due to a better control, respect to each individual therapy, of the pathogenetic mechanism of myocardia ischemia: BP and HR increases during exercise and during symptomatic ischemic episodes are controlled by the beta-blocker and coronary vasoconstriction during silent ischemia is prevented by the calcium-antagonist.