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.

[Hereditary changes of apolipoproteins B and E]. / Alterazioni ereditarie delle apolipoproteine B ed E.

Accelerated atherosclerosis occurs in patients with type III hyperlipoproteinemia and familial hypercholesterolemia. The accumulation of chylomicron remnants of intestinal origin and of VLDL remnants or IDL of hepatic origin observed in type III hyperlipoproteinemia appears to correlate with coronary disease. The presence of defective forms of Apo E prevents normal receptor-mediated catabolism of these lipoproteins. Patients with familial hypercholesterolemia have an elevation of plasma IDL secondary to defective LDL receptors that impair normal catabolism. Familial defective Apo B100 is secondary to an abnormality of Apo B100 that prevents the normal interaction of LDL with the LDL receptor and increases plasma LDL. Macrophages (which are derived from circulating monocytes) have emerged as a key component in atherogenesis because they appear to be progenitors of foam cells in arterial lesions. Macrophages express receptors that recognize chylomicron remnants and VLDL remnants and chemically modified LDL. Thus, in the presence of these specific lipoproteins, macrophages are converted to cells that resemble foam cells.

[Lipoprotein metabolism in arterial walls and its relationship with the genesis of atheromatous lesion]. / Il metabolismo delle lipoproteine nella parete arteriosa e suoi rapporti con la genesi della lesione ateromatosa.

In this review we have concentrated on the ways in which modification of LDL structure may account for foam cell formation. We have presented in vivo evidence as well as in vitro evidence supporting the proposition that modification of native LDL is a prerequisite for foam cell formation and atherogenesis. If further research supports the importance of LDL modification in atherogenesis, a whole new array of possibilities opens itself to us for intervention. At the moment, the only intervention that appears to be feasible is prevention of LDL oxidation; conceivably we might be able to interfere with the aggregation of LDL with itself or with other complexes in the artery wall that appear also to favor initiation of the atherogenic process.

Echo-Doppler evaluation of diastolic filling in differently induced left ventricular hypertrophy.

The study was performed in order to assess whether left ventricular hypertrophy (LVH) (exercise or pressure-overload induced but of a similar extent) may differently affect LV diastolic function. The authors compared LV filling echo-Doppler indexes of 16 male trained rowers (mean left ventricular mass index (LVMI) = 162 +/- 18 g/m2) with those of 34 male patients with secondary LVH, subdivided into two groups according to the extent of LVH (group I, n = 20, with a mean LVMI = 159 + 20 g/m2, and group II, n = 14, with a mean LVMI = 221 +/- 23 g/m2). No abnormalities of LV diastolic filling were observed in the athletes; while in patients with secondary LVH of group I an impairment of the echo-Doppler indexes was detected. A more severe involvement of the diastolic properties was observed in patients with LVH of group II.

A biochemical method for the quantitation of myocardial scarring after experimental coronary artery occlusion.

The histologic examination and planimetric evaluation of tissue slices has been so far the only available technique for studying the extent of experimental myocardial infarcts in long-term studies; however, this approach is rather time-consuming when the sample size is large. This study describes a new biochemical method for the quantitation of myocardial scarring, based on the determination of left ventricular hydroxyproline, and collagen content at the end of the healing process. Accordingly, several modifications were introduced into previously existing methods for the assay of hydroxyproline: our method allows a linear estimation of hydroxyproline in the range from 0.5 to 5 micrograms, with a precision of +/- 6.1% and a day-to-day variation of +/- 10.5%. The reliability of this approach for studying infarct size has been verified in rats with coronary artery occlusion divided into a control group and in a treated group receiving nitroglycerin. The animals were killed 21 days after coronary ligation and randomly assigned for infarct size evaluation either to the histologic or the collagen method. By histology infarct size averaged 30.6 +/- 4.8% (mean +/- S.E.M.) of left ventricle (LV) in control rats and 16.2 +/- 5.8% of LV in nitroglycerin-treated animals; by the proposed alternative method left ventricular collagen content was 26.8 +/- 1.0 micrograms/mg of dry weight in control rats and 19.5 +/- 1.2 micrograms/mg of dry weight in nitroglycerin-treated animals; infarct size calculated from collagen content by a simple formula, was 37.4 +/- 2.6% of LV and 22.3 +/- 2.6% of LV, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Asymptomatic transient ST changes during ambulatory ECG monitoring in diabetic patients.

The reported higher incidence of painless myocardial infarction in diabetic patients suggests that asymptomatic transient myocardial ischemia may also be frequent in diabetes. To explore this possibility 51 subjects with type II diabetes, aged 43 to 71 years (mean +/- SEM 56 +/- 8), 70 nondiabetic patients with coronary artery disease (mean age 55 +/- 5), and 40 nondiabetic patients without overt coronary disease (age 54 +/- 9) were studied. Thirty-eight of the 51 diabetic patients (74%) had evidence of associated coronary disease and 19 (37%) had evidence of previous myocardial infarction. All subjects underwent continuous 24-hour ambulatory ECG monitoring. In 18 of 51 diabetic patients 93 episodes (73% of the total number) of asymptomatic ST segment changes were recorded; the total number of symptomatic episodes was 36, and they were observed in seven patients (27%). Forty-eight (60%) asymptomatic and 32 symptomatic episodes of significant ST changes were found in nondiabetic patients with coronary artery disease. When patients with previous myocardial infarction were examined separately, asymptomatic episodes of significant ST changes were observed in 10 of 19 diabetic patients and in 5 of 25 nondiabetic patients with coronary artery disease (p less than 0.05). In an additional 28 diabetic patients who underwent exercise stress test, 15 exhibited an abnormal ECG response; however, only five of them (33%) were symptomatic. This study suggests that the incidence of transitory myocardial ischemia, as assessed by ambulatory ECG monitoring and exercise stress test, is higher in type II diabetic patients than in nondiabetic control subjects with coronary artery disease.