תוצאת חיפוש

Balloon Angioplasty of Native Coarctation of the Aorta

Benjamin Zeevi, Galit Bar-Mor, Michael Berant

Cardiac Catheterization Unit, Schneider Children's Medical Center, Petah Tikva, and Sackler School of Medicine, Tel Aviv University

The use of balloon dilatation to treat native coarctation of the aorta is gaining acceptance among interventional pediatric cardiologists, but is still controversial. We describe our experience with this procedure in 21 children, mean age 5.6 years and mean weight 21.1 kg. Most had an additional congenital heart defect, most commonly a bicuspid aortic valve. 17 were asymptomatic, 3 had tachypnea and 1 infant had severe congestive heart failure and was ventilated. The mean systolic blood pressure was 129.7 mm Hg.

Balloon dilatation was successful in 90% (19), decreasing the mean maximal systolic gradient from 35.3 to 9 mm Hg (p<0.001), and increasing the narrowest area from 3.9 to 8.2 mm (p<0.001), with a mean balloon-to-coarctation width-ratio of 2.8. There were no complications. Of 15 who underwent repeat cardiac catheterization at a mean interval of 10.6 months, 2 had a maximal systolic gradient of more than 20 mm Hg. 1 of these underwent successful repeat angioplasty and the other, who also had a small aneurysm, underwent surgical repair successfully. 2 others had small aneurysms and they are being followed clinically.

All patients were seen again after a mean interval of 31 months. The mean systolic blood pressure was 104 mm Hg, significantly lower than before intervention (p<0.002). 1 had an increased pressure gradient between right arm and leg of 35 mm Hg at later follow-up, and repeat cardiac catheterization demonstrated a good result 13 months after the initial procedure. She is awaiting a third catheterization. Overall, 90% had good mid-term results.

Based on our experience and recent reports, balloon angioplasty is safe and effective in most children older than 7 months and should be considered a viable alternative to operation for discrete aortic coarctation. Further long-term evaluation is needed.

Pulmonary Hypertension and Multi-Valvular Damage Caused by Anorectic Drugs

Serge E. Goldstein, Yair Levy, Yehuda Shoenfeld

Medical Dept. B and Institute for Immunological Disease Research, Chaim Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University

Marked obesity is an independent risk factor for multisystem morbidity. The use of anorectic drugs is an aggressive strategy for weight reduction. It appears to be an easy way of dealing with the problem, because the patient needn't change his behavior. However, such treatment is not harmless. At the end of the 60's an outbreak of pulmonary hypertension was associated with the drug aminorex, and it was soon withdrawn from the market. 30 years later it became clear that new-generation anorectic drugs (fenfluramine, dexfenfluramine, phentermine), which were being used world-wide, lead to both pulmonary hypertension and valvular damage.

We describe a woman of 70 with both these complications which developed after prolonged anorectic therapy with a fenfluramine-phentermine combination.

Mechanism of Primary Hypertension

Ludwig Kornel,* Arthur V. Prancan

Steroid Research Laboratory, Depts. of Internal Medicine and Biochemistry, and Dept. of Pharmacology, Rush Medical Center, Chicago and *Endocrinology-Diabetes Outpatient Clinic, Kupat Holim Klalit, Jerusalem

We review various theories of the pathogenetic mechanisms of steroid-induced and essential hypertension. We investigated the possibility that a pathogenetic mechanism leading to glucocorticoid (GC)-induced hypertension or to mineralocorticoid (MC)-induced hypertension, or both, may be of critical importance in primary hypertension. We studied plasma levels of corticosterone (BK) and aldosterone (Aldo), and their concentrations in arterial and renal tissues of spontaneously hypertensive rats (SHR), a model of primary hypertension, and in the antecedent strain WKY rats as a normotensive control. Plasma levels of BK and Aldo were found to be normal and identical in SHRs and WKYs. Tissue (intracellular) levels of BK were more than double in SHRs than in WKYs. Subsequently we examined the activity of 11b-hydroxy steroid dehydrogenase (11-HSD) in both aortic and renal tissues of SHRs and WKYs. 11-HSD converts BK to the corresponding 11-keto compound, 11-dehydro-corticosterone (cpd.AK), which is inactive, in view of its inability to bind to the MC receptors (and also to the GC receptors). BK, the main glucocorticoid in the rat, as well as cortisol, have high affinity for the MC-receptor (MR). Normally BK or cortisol are present in 10²-10³ times greater concentrations than Aldo in tissues possessing MR. The enzyme 11-HSD deactivates BK (or cortisol), thus protecting MC-receptors in the MC target tissues from being activated by GC. When we examined arterial and renal tissue activities of 11-HSD in SHRs, the activity of 11-HSD was only one-third that found in the WKY rats. This explained higher levels of BK in the tissues of SHR, and suggested that decreased activity of 11-HSD is a pathogenetic factor for hypertension in SHRs.

Thus, in a model of primary hypertension such as SHR, decreased activity of 11-HSD in the target tissues of MC appears to lead to glucocorticoid-induced mineralocorticoid hypertension.

Orthostatic Hypotension as a Manifestation of Malignant Lymphoproliferative Disease

H. Semo, A. Adunsky, E. Grossman

Depts. of Geriatric Medicine and of Medicine D, Chaim Sheba Medical Center, Tel Hashomer

An 85-year-old man was admitted with 6-month history of incapacitating orthostatic hypotension. Investigation led to the discovery of sympathetic dysautonomia, sensorimotneuropathy and malignant lymphoproliferative disease. Several attempts to treat the orhypotension or the neoplastic disease failed to improve his condition. Orthostatic hypotension precipitated by sympathetic dysautonomia may be an infrequent effect of early malignant lymphoproliferative disease.

Red Cell Na+/H+ Exchange and Role of Protein Kinase C in its Stimu-Lation in Diabetes Mellitus, Essential Hypertension and Nephropathy

Wladimir Koren, Robert Koldanov, Edna Peleg, Eva Izsak, Meir Berezin, Talma Rosenthal

Dept. of Medicine C, Hypertension Unit and Endocrinology Institute, Chaim Sheba Medical Center, Tel Hashomer

Na+/H+ exchange (NHE) was measured as maximal initial velocity of pH-dependent H+ efflux from red cells into an alkaline medium containing Na+ in patients with insulin-dependent or noninsulin-dependent diabetes, with and without hypertension and in normoglycemic, essential hypertensives and normal controls (50 subjects in each subgroup). Maximal velocities of NHE were found in microalbuminuric patients in all subgroups, and NHE correlated with the rate of microalbuminuria (r=0.61, p=0.02). Daily insulin requirements were greater in those with elevated NHE (84±8 vs 42±4 U/day). There was no correlation between NHE and levels of plasma glucose, HbA1 and plasma aldosterone and lipid profile and PRA. NHE was correlated with plasma prolactin (r=0.51, p=0.02) and PTH r=0.24, p=0.05). In uremic patients, NHE was inversively correlated with creatinine clearance (r=-0.48, p=0.03). Since calphostin C, a selective inhibitor of protein kinase C, lowered increased NHE in vitro, the protein kinase C-dependent pathway of the exchanger regulation was concluded to be responsible for NHE activation in diabetes mellitus and essential hypertension.

Ischemic Hepatitis in Congestive Heart Failure after an Episode of Hypotension

Ora Shovman, Jacob George, Yehuda Shoenfeld

Dept. of Medicine B and Autoimmune Disease Clinic Research Unit, Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University

Ischemic hepatitis can occur as an acute episode in advanced congestive heart failure (CHF). The mechanism is massive necrosis of the central lobules resulting from acute hypoxia when low cardiac output further reduces oxygen supply, aggravating underlying congestion due to poor venous outflow. We describe a 70-year-old woman with congestive heart failure for 7 years who was admitted with jaundice, vomiting, abdominal pain and oliguria after an episode of hypotension. The diagnosis of ischemic hepatitis was established by a documented episode of severe hypotension, followed by elevation of serum transaminases, a rise in serum bilirubin and LDH levels, prolonged prothrombin time and acute renal failure. Other causes of acute hepatitis, such as a virus or drugs were excluded, and improved liver and renal function followed hemodynamic stabilization. We conclude that ischemic hepatitis should be considered whenever acute hepatitis follows a recent episode of systemic hypotension, especially in the context of concomitant CHF.