Infrarenal aortic stenosis: value of stent placement after percutaneous transluminal angioplasty failure.

PURPOSE: To evaluate the long-term clinical and hemodynamic effectiveness of aortic stent placement in cases of failure of intended infrarenal percutaneous transluminal aortic angioplasty (PTAA). MATERIALS AND METHODS: Fifty-three patients who underwent technically successful PTAA were compared with 24 patients who underwent aortic stent placement because of PTAA failure (19 patients) or ulcerated lesions (five patients) that otherwise would have been treated surgically because of the embolization hazard associated with PTAA alone. Clinical patency was defined as the absence or improvement of symptoms after the intervention. Hemodynamic patency was defined as a normal Doppler waveform in the common femoral arteries, an ankle-brachial index greater than 0.95, or the absence of a thigh-brachial pressure gradient. RESULTS: Three-year clinical and hemodynamic patency rates, respectively, were 85% and 79% for PTAA and 69% and 43% for aortic stent placement. No morbidity was encountered. With use of the Cox proportional hazards model, two significant risk factors were retained for restenosis: unchanged smoking habit (P =.04) and small dilatation diameter (P =.001). Aortic stent placement, performed in patients with a smaller aortic diameter (10.3 vs. 12.7 mm for PTAA), appeared to be a predictive factor for restenosis by using univariate analysis. By using the Cox proportional hazards model, however, the restenosis rates after PTAA and aortic stent placement were not significantly different. CONCLUSION: When aortic diameter is taken into consideration, there is no evidence that clinical outcome after secondary aortic stent placement would be poorer than technically successful PTAA.

[Calcium channel blocking agents and albuminuria in diabetic and hypertensive patients. A pilot study]. / Agents bloqueurs des canaux calciques et albuminurie des sujets diabétiques et hypertendus. Une étude pilote.

UNLABELLED: Diltiazem tends to decrease proteinuria in hypertensive diabetic subjects in comparison to amlodipine that does not modify it. Since estimated glomerular pressure is identical in amlodipine treated and diltiazem treated subjects, differences in albuminuria may be explained by different renal tubular reabsorption rates. OBJECTIVES: To compare plasma clearances (PC) of technetium labeled albumin (albumin-Tc99m) obtained by serial plasma measurements with PC obtained by urinary excretion measurements. Indirectly evaluate tubular reabsorption of albumin-Tc99m. Test the hypothesis that amlodipine decreases renal tubular reabsorption of albumin in diabetic hypertensive subjects. METHODS: Fourteen diabetic and hypertensive subjects (DH) (average plasma creatinine: 94 mmol/L) and 6 normal subjects (average plasma creatinine: 82 mmol/L) had previously been assessed for albumin-Tc99m PC. Eleven of these 14 DH subjects were then randomized to diltiazem 300 mg/daily (6 subjects) or amlodipine 10 mg/daily (5 subjects). Their glomerular filtration, glomerular pressure and albumin-Tc99m PC were then assessed on the 3rd, 6th, and 12th month of the study. RESULTS: Albumin-Tc99m PC obtained from serial blood draws: A decrease in PC between months 0 and 3 from 14 to 10.6 cc/min was observed in subjects treated with amlodipine but subjects on diltiazem showed PC stability (from 11.9 to 12 cm3/min). PC obtained from urinary excretion: Amlodipine and diltiazem treated subjects showed PC stability. Plasma volume in amlodipine treated subjects decreased from 156 to 127% and diltiazem treated subjects from 128 to 117%. CONCLUSION: A decrease in PC obtained with plasma measurements and stability of PC based on urinary excretion measurements tends to identify a decrease in plasma volume. A decrease in albumin-Tc99m tubular reabsorption was not observed. The estimate of albumin PC with Tc 99m labelled albumin measurements still needs to be validated.

Different effects of nifedipine and amlodipine on circulating catecholamine levels in essential hypertensive patients.

OBJECTIVE: To compare the acute and chronic effects of nifedipine retard (NPA), nifedipine gastrointestinal therapeutic system (NGITS) and amlodipine at trough and peak plasma concentrations of drug on blood pressure and heart rate, and on plasma norepinephrine and epinephrine levels in patients with mild-to-moderate hypertension (diastolic blood pressure 95-115 mmHg). DESIGN AND METHODS: After 3-4 weeks' placebo treatment, patients of both sexes were randomly allocated to be administered 10 or 20 mg NPA twice a day, 30 or 60 mg NGITS once a day, and 5 or 10 mg amlodipine once a day for 6 weeks. Initially, for the first 2 weeks, the lowest dose of each drug was used, but higher doses were administered after 2 weeks if sitting diastolic blood pressure was > 90 mmHg. Patients were evaluated after administration of the first dose and after 6 weeks' therapy in a hospital setting. Blood samples were taken for high-performance liquid chromatography measurement of catecholamine and drug levels at various intervals for a period covering trough to peak drug level ranges. RESULTS: Administration of all three drugs reduced clinic blood pressure to the same level after 6 weeks' therapy, but heart rate was increased slightly only with amlodipine (P < 0.05). Administration of NPA reduced blood pressure more abruptly whereas administrations of NGITS and amlodipine induced smoother falls after acute and chronic treatments: a significant increase in heart rate was observed with amlodipine after chronic treatment. Both acute and chronic treatments with NPA (n = 19) increased norepinephrine levels (P < 0.01) transiently (2-4 h). In contrast, administration of NGITS (n = 22) did not increase norepinephrine levels and even induced a slight but significant decrease in norepinephrine levels 5-6 h after chronic treatments. Although administration of amlodipine (n = 22) did not increase norepinephrine levels transiently either after acute or after chronic administration, it did induce a sustained rise in basal norepinephrine levels by more than 50% after chronic therapy (P < 0.01). Plasma epinephrine levels were not increased by any of the treatments and even a slight decrease was observed 4 h after administration of a dose following chronic treatments with NGITS and amlodipine (P < 0.05). CONCLUSIONS: The transient increase in norepinephrine levels observed with NPA and the sustained increases in norepinephrine levels observed after chronic treatment with amlodipine suggest that sympathetic activation occurs with those two drugs. The lack of increase in norepinephrine levels after administration of NGITS suggests that this formulation does not activate the sympathetic system. The lowering of epinephrine levels after administrations of NGITS and amlodipine suggests that inhibition of release of epinephrine by the adrenal medulla occurs with longer-acting dihydropyridine formulations.

Infrarenal aortic stenosis: long-term clinical and hemodynamic results of percutaneous transluminal angioplasty.

PURPOSE: To evaluate the safety and long-term clinical and hemodynamic results of percutaneous transluminal angioplasty (PTA) of the infrarenal aorta. MATERIALS AND METHODS: During nearly 10 years, 102 patients with symptomatic infrarenal atherosclerotic aortic stenosis underwent PTA. Follow-up information was available in 92 patients (17 men, 75 women; mean age, 51.9 years). Stenosis involved the aortic bifurcation in 18 patients and only the infrarenal abdominal aorta in 74 patients. Technical success was defined as residual stenosis less than 50% or a pressure gradient less than 10 mm Hg after PTA. Clinical patency was defined as the absence or improvement of symptoms after PTA. Hemodynamic patency was defined as a normal Doppler waveform in the common femoral arteries, an ankle-brachial ratio greater than 0.95, or the absence of a thigh-brachial pressure gradient. RESULTS: Technical success was achieved in 78 patients after PTA. After 10 years, primary clinical and hemodynamic patency rates were 72% and 46%, respectively. After a mean follow-up of 51 months, 15 of the 22 symptomatic recurrences were due to aortic restenosis; 11 of these were treated with repeated PTA with or without stent placement, and three eventually required aortic surgery. No morbidity was encountered. CONCLUSION: Infrarenal aortic PTA proved to be safe and provided durable, long-term clinical improvement. In this group of relatively young patients, the clinical patency rate of PTA was equivalent to that of aortic surgery but with less morbidity.

Different effects of nifedipine and amlodipine on circulating catecholamine levels in essential hypertensive patients.

OBJECTIVE: To compare the acute and chronic effects of nifedipine retard (NPA), nifedipine gastrointestinal therapeutic system (NGITS) and amlodipine at trough and peak plasma concentrations of drug on blood pressure and heart rate, and on plasma norepinephrine and epinephrine levels in patients with mild-to-moderate hypertension (diastolic blood pressure 95-115 mmHg). DESIGN AND METHODS: After 3-4 weeks' placebo treatment, patients of both sexes were randomly allocated to be administered 10 or 20 mg NPA twice a day, 30 or 60 mg NGITS once a day, and 5 or 10 mg amlodipine once a day for 6 weeks. Initially, for the first 2 weeks, the lowest dose of each drug was used, but higher doses were administered after 2 weeks if sitting diastolic blood pressure was > 90 mmHg. Patients were evaluated after administration of the first dose and after 6 weeks' therapy in a hospital setting. Blood samples were taken for high-performance liquid chromatography measurement of catecholamine and drug levels at various intervals for a period covering trough to peak drug level ranges. RESULTS: Administration of all three drugs reduced clinic blood pressure to the same level after 6 weeks' therapy, but heart rate was increased slightly only with amlodipine (P < 0.05). Administration of NPA reduced blood pressure more abruptly whereas administrations of NGITS and amlodipine induced smoother falls after acute and chronic treatments: a significant increase in heart rate was observed with amlodipine after chronic treatment. Both acute and chronic treatments with NPA (n = 19) increased norepinephrine levels (P < 0.01) transiently (2-4 h). In contrast, administration of NGITS (n = 22) did not increase norepinephrine levels and even induced a slight but significant decrease in norepinephrine levels 5-6 h after chronic treatments. Although administration of amlodipine (n = 22) did not increase norepinephrine levels transiently either after acute or after chronic administration, it did induce a sustained rise in basal norepinephrine levels by more than 50% after chronic therapy (P < 0.01). Plasma epinephrine levels were not increased by any of the treatments and even a slight decrease was observed 4 h after administration of a dose following chronic treatments with NGITS and amlodipine (P < 0.05). CONCLUSIONS: The transient increase in norepinephrine levels observed with NPA and the sustained increases in norepinephrine levels observed after chronic treatment with amlodipine suggest that sympathetic activation occurs with those two drugs. The lack of increase in norepinephrine levels after administration of NGITS suggests that this formulation does not activate the sympathetic system. The lowering of epinephrine levels after administrations of NGITS and amlodipine suggests that inhibition of release of epinephrine by the adrenal medulla occurs with longer-acting dihydropyridine formulations.