Alessio Calabrò

Carotid artery lesions in patients with nondiabetic chronic renal failure

Atherosclerotic complications are the leading cause of death in chronic renal failure (CRF) patients. Therefore, we wished to investigate the prevalence of carotid artery lesions (CALs) in these subjects. Two groups were evaluated by high-resolution echo Doppler: group 1 included 103 patients (68 males and 35 females) affected by nonnephrotic CRF and group 2 included 100 control subjects (60 males and 40 females). The prevalence of hypertension was 84% in both groups. The exclusion criteria included diabetes mellitus and symptoms of cerebrovascular disease. In the two groups we evaluated clinical history, physical examination, total cholesterol, triglycerides, fibrinogen, blood cell counts, blood urea nitrogen, creatinine, 24-hour proteinuria, and urine analysis. In group 1 patients the following lipid profile parameters were also evaluated: low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, lipoprotein(a), ApoAI, ApoAII, and ApoB. Group 1 had higher triglycerides and fibrinogen than group 2. A lower body mass index was found in group 1 than in group 2. The prevalence of CALs was significantly higher in the CRF patients than in the control subjects (62% v 47%; P = 0.04). The difference between the two groups was more striking among normotensive patients (62% v 19%; P = 0.03). All CRF patients affected by peripheral arterial disease and 86% of those having coronary artery disease had associated CALs. In CRF patients the severity of CALs was positively correlated to age, white blood cell count, triglycerides, and fibrinogen. Nondiabetic CRF patients have a higher prevalence of carotid artery lesions than control subjects. Several factors besides hypertension, including lipids, blood coagulation, and leukocytes, could contribute to the accelerated atherosclerosis of CRF patients.

Carotid artery endarterectomy in patients with contralateral carotid artery occlusion: Perioperative hazards and late results

The aim of this study was to analyze and compare the perioperative hazards and late results of internal carotid endarterectomy (CEA) in patients with and without contralateral internal carotid artery occlusion. From March 1980 to April 1990, 375 consecutive patients underwent 439 CEAs at the First Department of Vascular Surgery of Padova Medical School. Patients were divided into two groups; group 1 (61 patients) had contralateral internal carotid artery occlusion and group 2 (314 patients) did not (378 CEAs, 64 bilateral). Indications for CEA were similar in both groups. The only significant difference in patient characteristics was a higher rate of previous stroke in group 1 (11% vs. 3%,p< 0.001). General anesthesia, continuous EEG monitoring, selective intraluminal shunt, and arteriotomy closure with a polytetrafluoroethylene patch (PTFE) were used routinely in both groups. An intraluminal shunt was inserted more frequently in group 1 than in group 2 (69% vs. 17%,p<0.001). Major perioperativestroke occurred in one patient in each group (1.7% vs. 0.31%, respectively; NS). Early fatal stroke rates were 0% and 0.95% in groups 1 and 2, respectively (NS). All patients had neurologic examinations and duplex scans every 6 months (range 6 to 118 months; mean 42 months). Kaplan-Meier survival curves were virtually identical in the two groups; the majority of deaths were caused by myocardial infarction and cancer. There were no stroke-related deaths in group 1 as compared with 8.2% in group 2 (NS). New neurologic symptoms appeared in 4.7% of patients in group 1 and 6% in group 2 (NS) whereas the late stroke rates were 0% and 3.1%, respectively (NS). Restenosis was observed in two and three patients in groups 1 and 2, respectively (NS). In conclusion, CEA for ulcerated or stenotic lesions of the internal carotid artery in patients with contralateral carotid occlusion is associated with very low early and long-term neurologic morbidity and mortality, similar to findings in patients who undergo CEA with a patent contralateral carotid artery.

The renin-angiotensin-aldosterone system and carotid artery disease in mild-to-moderate primary hypertension.

Background The evidence linking activation of the renin— angiotensin system with accelerated cerebro-vascular atherosclerosis remains controversial. We therefore prospectively investigated the relationships of plasma renin activity and aldosterone levels with carotid artery lesions (CAL) in essential hypertension. Methods We evaluated the prevalence and severity of CAL and the intimal—medial thickness (IMT) with a high-resolution echo-Doppler technique in 107 cerebrovascularly asymptomatic consecutive primary hypertensives (55 male, 52 female) and in 70 (42 male, 28 female) normotensive controls. We also measured supine plasma renin activity (PRA) and aldosterone before and 45 min after captopril administration, while daily urinary excretion of sodium was measured. Results Both the prevalence (59.4 versus 26.2%) and severity of sex- and age-adjusted and unadjusted CAL and IMT were significantly higher in hypertensives than in controls. Regression analysis showed different predictors of IMT (age and captopril-stimulated-PRA, R2 = 0.27, P < 0.0001), score of CAL (mean blood pressure, R2 = 0.15, F = 12.73, P < 0.0001) and maximal stenosis (pulse pressure and known duration of hypertension R2 = 0.29, F = 14.58, P < 0.0001). Sex- and age-adjusted IMT did not differ between quartiles of renin-sodium profile. However, patients in the quartile with the highest PRA had the lowest score of CAL and an inverse relationship between age-adjusted PRA and IMT and CAL was found. Conclusions These results, besides confirming an association of both IMT and CAL with primary hypertension and ageing, demonstrate that CAL and IMT have different correlates. However, they do not support the contention that a high renin-sodium profile carries an excess risk of CAL in primary hypertensives with no clinical evidence of cerebro-vascular disease.

Clinical Assessment of Low Molecular Weight Heparin Effects in Peripheral Vascular Disease

This study was carried out, using the double-blind method vs placebo, on 36 patients suffering from stage II peripheral vascular disease (PVD) according to Leriche, to check the clinical and hemorrheologic effects of the administration of a new low molecular weight heparin (LMWH). After a one-month washout period, the patients were randomly assigned either to the group treated with the LMWH (15,000 aXaU/day sc) or to the group treated with indistinguishable placebo. At the start of the study and after three and six months of treatment, clini cal, instrumental, and laboratory tests were performed to assess local and sys temic efficacy and tolerance. The LMWH under study caused a statistically significant increase in claudi cation time, with a parallel increase in the absolute claudication distance and in the interval free of pain. The drug also led to a significant increase in activated partial thromboplastin time, the values of which, however, remained within the normal limits, and to a marked reduction in blood viscosity. No significant vari ation was observed in the tolerability parameters in the two treatment groups, and no local or systemic adverse reactions occurred.

Relationship of Early Carotid Artery Disease With Lipoprotein (a), Apolipoprotein B, and Fibrinogen in Asymptomatic Essential Hypertensive Patients and Normotensive Subjects

Abstract Background We investigated the relationships between plasma lipids and lipoprotein fractions and carotid artery lesions (CAL) in 177 cerebro-vascularly asymptomatic subjects, of whom 107 were primary hypertensive patients and 70 normotensive controls. Methods The prevalence and severity of CAL, as assessed by calculating a score of severity (score of CAL) and the maximal stenosis of both sides, as well as the intimal-medial thickness (IMT) were evaluated with a high-resolution echo-Doppler technique. We measured total serum cholesterol, triglycerides, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, lipoprotein (a) [Lp(a)], Apo (apolipoprotein)AI, ApoAII, ApoB, and fibrinogen. Results Both the prevalence (59.4% vs 26.2%) and severity of sex- and age-adjusted and unadjusted CAL and IMT were significantly higher in hypertensive patients than in controls. Regression analysis showed different predictors of IMT and maximal stenosis. The variables that remained in the model were age, mean blood pressure (BP), and smoking for IMT; pulse pressure, known duration of hypertension (HT), fibrinogen, and ApoB for the score of CAL; and the last four variables along with age and mean BP for maximal stenosis. Furthermore, we identified a link between the atherogenic lipoprotein fractions Lp(a) and ApoB, fibrinogen and early carotid artery atherosclerotic changes. Conclusions The different correlates of IMT, CAL, and maximal degree of stenosis suggest that they reflect different events occurring in the arterial wall in response to aging, HT, and other risk factors, rather than simply different stages of the same atherosclerotic process.

Stroke risk reduction in asymptomatic and symptomatic patients treated surgically: The effectiveness of carotid endarterectomy with patch graft angioplasty

From March 1980 to March 1987, 217 consecutive patients underwent 252 carotid revascularisations with routine use of continuous EEG monitoring and selective use of an intraluminal shunt for symptomatic (70%) or asymptomatic (30%) internal carotid artery (ICA) atherosclerotic stenosis. All carotid endarterectomies were routinely performed with a patch graft angioplasty. None of the patients suffered permanent or transient neurological deficits in the immediate postoperative period and none of them died. There was an 0.8% stroke rate and 0.4% mortality rate in the early postoperative course. Neurological assessment, Doppler and Echo doppler sonography of both the operated and the contralateral ICA was performed every 6 months. One-hundred and twenty-one patients (142 carotid revascularisations) operated on up to December 31st 1985 were reassessed in July 1986. The mean follow-up time was 35 months (range: 6 months to 6 years). New neurological symptoms were present in 7.4% of the patients; 2.5% of patients developed a stroke and 8.9% showed progression of stenosis in the contralateral ICA. One patient had a common carotid artery stenosis 2 years after surgery. Re-stenosis of the ICA was found in two patients who underwent re-operation without difficulty. The late mortality was 21.4% (11.9% of the overall series). In only two patients (7.6%) was stroke the cause of death.

The Hemodynamic Abnormalities in Short-Term Insulin Deficiency: The Role of Prostaglandin Inhibition

It has been suggested that the hemodynamic derangements present in diabetic ketoacidosis are the results not only of profound volume depletion but also of the effects of increased production of vasodilating prostaglandins (PGs), principally PGI2, released by adipose tissue. In animal and in vitro models, prostaglandin synthesis is increased during insulin deficiency. We assessed the effects of short-term ketosis on the metabolic and hemodynamic variables of 10 IDDM patients free from long-term complications and of 9 normal control subjects after a 7-day randomized double-blind indomethacin (INDO) (50 mg q.i.d.) or placebo treatment period. Calf blood flow (CBF), postocclusive reactive hyperemia (PORH), and recovery half-time (an index of overall perfusion) after PORH were measured by plethysmography. Left ventricular and myocardial functions were also studied in each different condition during placebo and INDO treatment in IDDM patients. During placebo treatment, the increase in CBF during ketosis was higher (1.75 ± 0.29 ml · min−1 · 100 ml muscle−1) than during INDO (0.85 ± 0.17 ml · min−1 · 100 ml muscle−1; P = 0.007). PORH was similar in baseline conditions, during ketosis, and in recovery in both the placebo and INDO arms. Recovery half-time significantly increased during placebo (10 ± 2; 200%; P < 0.01) but not during INDO (1 ± 1; 106%; NS) treatment. In normal control subjects, insulin deficiency did not induce any significant effect on hemodynamic variables. In IDDM patients, during placebo treatment, ketosis increased both the cardiac index (from 3.4 ± 0.7 to 4.1 ± 0.8 1 · min−1 · m−2; P < 0.01) and the stroke index (from 42 ± 8 to 49 ± 7 ml/m2; P < 0.01) without changes in left ventricular ejection fraction but with a significant increase in both left and right ventricular end-diastolic volumes. Metabolic recovery induced a normalization of these parameters. INDO treatment significantly blunted these alterations. In summary, we showed that during acute insulin deficiency, INDO-sensitive mechanisms mediate vascular disturbances. Moreover, INDO treatment was capable of completely preventing the cardiac venous return and the left ventricular alterations. INDO does not interfere with the overall ketogenetic process or with insulin-induced metabolic recovery.