Beneficial effect of Bradycardia Tachycardia Response (BTR) algorithm on VT detection in the presence of rate smoothing.

INTRODUCTION: Rate smoothing algorithms, while known to help prevent ventricular tachyarrhythmias in some patients, have been shown to result in underdetection of ventricular tachycardia (VT) due to interaction between bradycardia pacing and tachycardia detection parameters. A new algorithm named Bradycardia Tachycardia Response (BTR) has been developed in order to prevent rate smoothing-induced underdetection. The efficacy of BTR is not known. The aim of this study was to assess the effectiveness of BTR in preventing VT underdetection due to rate smoothing. METHODS AND RESULTS: Two ICD models (TELIGEN and VITALITY AVT, Boston Scientific, St. Paul, MN, USA) bearing identical rate smoothing algorithms were connected to a VT simulator. Devices were programmed similarly except for the BTR feature that exists in TELIGEN only. The detection performance of both devices was tested using varying combinations of AV delay, rate smoothing down, and upper rate limit and compared between the two models. VT underdetection (delay or nondetection) occurred during pacing in 62% of the VT episodes with VITALITY AVT. In TELIGEN, all simulated VT episodes were detected appropriately as soon as their rates exceeded the programmed VT detection rate. Detection tended to be affected by higher upper rate, longer AV delays, and more aggressive rate smoothing. CONCLUSION: The BTR algorithm effectively counteracts VT detection delay caused by the interaction of rate smoothing with VT detection parameters, thus enabling safe use of the rate smoothing feature.

Cardiac troponin I in patients with acute lower limb ischemia.

The presence, cause, and clinical significance of elevated cardiac troponin I in patients with acute lower limb ischemia is yet unknown. Forty-six patients (20 men [43%]; mean age 72 +/- 10 years, range 42 to 92) with acute lower limb ischemia were enrolled in this study. Serial creatine kinase (CK), CK isoenzyme MB (CK-MB), and troponin I measurements were obtained in all consecutive patients. Peak levels were evaluated for each patient. Twenty-four patients (52%) had elevated peak troponin I levels (>0.2 ng/ml) during their hospitalization. Patients were divided into 3 groups according to their peak troponin I levels: 11 patients (24%) had peak troponin I levels >1 ng/ml (the high troponin I group), 13 (28%) had levels of 0.2 to 1 ng/ml (the intermediate troponin I group), and the remaining 22 (48%) had peak troponin I levels <0.2 ng/ml (the low troponin I group). The peak CK levels were 10,263 +/- 16,513, 1,294 +/- 1,512, and 934 +/- 1,045 IU/ml (p = 0.04) in the 3 different troponin I subgroups, respectively, and the peak CK-MB levels were 143 +/- 170, 38 +/- 31, and 38 +/- 43, respectively (p = 0.04). Troponin I was positively correlated with CK (R = 0.35, p = 0.017) and CK-MB (R = 0.38, p = 0.009). The mean length of hospitalization was 8.3 +/- 6.2 days for the whole study group and did not vary among the 3 troponin I groups (10.5 +/- 10.9 vs 8.6 +/- 4.9 vs 7.2 +/- 4.0 days, p = 0.762). There were no differences in mortality during hospitalization among the 3 groups (4 of 11 vs 1 of 13 vs 4 of 22 patients, p = 0.22). In conclusion, patients with acute lower limb ischemia often have elevated cardiac troponin I levels. Elevated troponin I levels were not associated with the duration of hospitalization or with in-hospital mortality in this group of patients.

Statin treated patients have reduced intraplaque angiogenesis in carotid endarterectomy specimens.

BACKGROUND: Treatment with statins is considered a first line therapy in atherosclerotic disease. Intraplaque angiogenesis is involved in plaque progression and instability. It remains unclear whether the beneficial effect of statin treatment in humans is achieved through reduced intraplaque angiogenesis. The aim of this study was to evaluate the capillaries density in carotid plaques removed from patients treated with statin versus untreated patients. METHODS AND RESULTS: We studied 102 patients who underwent carotid endarterectomy: 98 of them met the inclusion criteria and entered the study; 75 men and 23 women; mean age 66+/-8 years (range 42-83 years). Forty-three patients (44%) were on statin treatment at least 3 months before endarterectomy and 55 (56%) had never received statin treatment. The intensity of intraplaque angiogenesis was evaluated with immunohistochemistry using the antibody CD34. The number of capillaries per mm(2) was measured with a custom designed image tool analysis. With the exception of serum total cholesterol levels and serum low-density cholesterol levels, the two groups of patients did not vary significantly in cardiovascular risk factors and in parameters pertaining to the procedure profile. Patients on statin treatment had less capillaries per mm(2) than patients not receiving this kind of drugs (0.97+/-0.61 per mm(2) versus 1.39+/-0.98 per mm(2), p=0.031). Univariate associations between possible explanatory variables and number of capillaries per mm(2) were tested using Spearman rank R. Variables associated with a p-value <0.20 (age, serum creatinine, serum total cholesterol, serum low-density lipoprotein, serum homocysteine, presence of diabetes mellitus and statin treatment) were entered in a multivariable model. Multivariate analysis showed that statin treatment was the only independent predictor (t=-5.39, p<0.001) of intraplaque angiogenesis. CONCLUSIONS: Statin therapy is associated with reduced intraplaque angiogenesis in the carotid arteries. This could provide an explanation for the beneficial effects of this kind of drug on patients with atherosclerotic disease.

Very late in-stent restenosis in a bare metal stent.

Restenosis after coronary artery stenting is a common phenomenon and represents a topic of great interest. Although a great volume of research is referring to restenosis, still many issues are not fully understood by the cardiological community. Here we present a case of very late restenosis, after a bare metal stent implantation.

Brain natriuretic peptide as marker of myocardial iron load in beta-thalassemia.

Cardiomyopathy due to iron overload represents a frequent life-limiting complication in patients with beta-thalassemia major. We have conducted a study which proved that brain natriuretic peptide plasma levels have high sensitivity and negative predictive value in detecting cardiac hemosiderosis.

Intravenous esmolol is well tolerated in elderly patients with heart failure in the early phase of non-ST elevation myocardial infarction.

AIM: To investigate the haemodynamic response to and clinical safety and tolerability of intravenous esmolol (Brevibloc), Baxter Healthcare Corporation, Deerfield, Illinois, USA) in elderly and younger patients with acute non-ST elevation myocardial infarction (NSTEMI) and heart failure. PATIENTS AND METHODS: We studied 24 consecutive patients, 12 of them elderly (> or =75 years old) and 12 younger (32-74 years old), with NSTEMI and symptoms of heart failure on presentation. After stabilisation of the patient's condition with standard therapy, intravenous esmolol was administered. An infusion rate of 0.05 mg/kg/min for 30 minutes was instituted and, if no adverse effects developed, this was increased to 0.20 mg/kg/min. All haemodynamic parameters were measured before and at the end of each administration using a Swan-Ganz catheter. RESULTS: Only one patient in the elderly subgroup did not tolerate the augmented infusion rate (because of severe bradycardia) and so had to return to the initial lower infusion rate. The cardiac index (mean +/- SD) was 2.4 +/- 0.9 L/min/m(2) at baseline and decreased to 1.9 +/- 0.4 L/min/m(2) (p < 0.05 vs baseline) at the end of the administration of the second dose of esmolol in the elderly patients and 2.6 +/- 0.5 L/min/m(2) and 2.2 +/- 0.5 L/min/m(2) (p < 0.05 vs baseline), respectively, in the younger patients. Mean pulmonary wedge pressure was 17 +/- 6mm Hg at baseline and increased to 19 +/- 4mm Hg (p < 0.05 vs baseline) at the end of the second dose of esmolol in the elderly patients and 16 +/- 10mm Hg and 18 +/- 10mm Hg (p < 0.05 vs baseline), respectively, in the younger patients. The response of both age groups to esmolol was the same for all of the parameters examined. CONCLUSION: Intravenous esmolol was safe and well tolerated in the early phase of NSTEMI in patients presenting with symptoms of heart failure and ongoing ischaemia, regardless of their age.