The effect of kidney transplant on cardiac function: an echocardiographic perspective.

Kidney transplant (KT) resolves many of the cardiac abnormalities associated with chronic kidney failure (CKF). This study analyzed cardiac alterations of kidney failure and their modification with transplant. Thirteen patients in CKF underwent conventional echocardiograms, dobutamine stress echocardiograms, and injection of contrast to examine perfusion before KT and 3 months after transplant. Nine patients had evidence of left ventricular hypertrophy and six had evidence of diastolic dysfunction. Wall thickness, left ventricular mass, and mass index diminished after KT; only two patients continued to manifest hypertrophy. Left ventricular systolic diameters and volumes diminished at 3 months, and diastolic diameters after 4 months. Left ventricular fractional shortening and ejection fraction increased 3 months after transplant. At the end of the study, only two patients continued to show diastolic dysfunction. Dobutamine echocardiograms showed no segmental wall-movement abnormalities. Myocardial perfusion was normal before and after transplant. The results suggest that KT diminishes hypertrophy and improves left ventricular systolic and diastolic function. Echocardiography provides valuable information for detection and follow-up of cardiac abnormalities in patients with kidney disease. Evaluation of segmental wall movement and myocardial perfusion aid in demonstrating that our studied patients with CKF had no indirect signs of coronary artery disease.

Fosinopril prevents hyperfiltration and decreases proteinuria in post-transplant hypertensives.

Hypertension and renal mass reduction induce glomerular hypertension (GH), hyperfiltration (HF) and renal injury. GH may contribute to allograft loss in post-transplant hypertensive patients (PT x HT). HF and GH may be evaluated by renal response to acute protein intake (API). Since ACE inhibition may prevent GH, the effects of fosinopril (Fos) were evaluated in 10 PT X HT on azathioprine and prednisone. Patients received 5 to 40 mg/day of Fos during 12 months. Baseline MAP (111.1 +/- 2.9 mm Hg) was significantly reduced by 10 to 12 mm Hg, rising to 114.7 +/- 2.7 mm Hg after Fos was administered. GFR (63.7 +/- 5.9 ml/min) decreased after 4 (48.1 +/- 4.6, P less than 0.05) and 12 months (50.7 +/- 4.6, P less than 0.05), rising to 59.4 +/- 5.6 after Fos was given. There was no GFR response to API before and after one month of Fos, however, a clear response became apparent at 4 (+ 27% P less than 0.05), and 12 months (+ 18%, P less than 0.05), disappearing after Fos discontinuation. Proteinuria (918.8 +/- 710.6 mg/d) decreased after 4 (72.3 +/- 21.6 mg/d, P less than 0.05) and 12 months, rising to 297.8 +/- 172.3 mg/day after therapy. GFR response to API in 22 controls and 17 uninephrectomized donors was 13 and 11%, respectively. Lack of response to API in PT x HT suggests HF and GH. Reduction of GFR, restoration of response to API and reduction of proteinuria, indicate that ACE inhibition with fosinopril ameliorates HF and GH. This effect may be beneficial in preventing hemodynamic-mediated allograft injury.

[Role of prostaglandins in the antihypertensive effect of the converting enzyme inhibitor, enalapril]. / Papel de las prostaglandinas en el efecto antihipertensivo del inhibidor de la enzima convertidora, enalapril.

Angiotensin converting enzyme (ACE) generates angiotensin II and is also capable of degrading bradykinin into inactive peptides. It has been suggested that the effects of ACE inhibitors are partially mediated by increased prostaglandin synthesis induced by a simultaneous rise in bradykinin. Captopril increases PG excretion and indomethacin (INDO) attenuates its effects. Enalapril is a long acting ACE inhibitor, and its molecule does not have the sulphydryl group present in captopril. In order to evaluate the participations of PG in a the ENA effects of enalapril (ENA) on arterial pressure (AP), plasma renin activity (PRA), plasma aldosterone (ALDO) and renal hemodynamics (RH) in essential hypertension (EHT), we compared the effects of ENA alone and associated with INDO. Nine EHT patients received on different occasions: ENA 10 mg, INDO 25 mg and ENA-INDO. Arterial pressure, PGE2, ALDO, PRA, RH and plasma and urinary ENA as enalaprylate were measured after each treatment. Maximal ENA absorption occurred after 4 hours, however it was still detectable after 72 hr. ENA decreased AP after 6 hr in spite of unchanged PGE2 excretion; PRA did not change and ALDO decreased transiently. INDO delayed ENA absorption, slightly attenuated the fall in AP and suppressed PGE2 excretion when given with ENA. INDO alone suppressed PGE2 and did not alter AP. No significant changes occurred in RH with the treatments. Our results suggest that the antihypertensive effect of ENA is independent of PG, and that the slight attenuation induced by INDO may be attributed to a delay in intestinal absorption. In EHT patients under normovolemic conditions, renal function is not altered by ACE inhibition.

[Evaluation of the efficacy and safety of dilevalol in the treatment of essential arterial hypertension]. / Evaluación de eficacia y seguridad del dilevalol en el tratamiento de la hipertensión arterial esencial.

Dilevalol, an optical isomer of labetalol, combines beta-blocking and vasodilator actions which prevent reflex tachycardia and it also has intrinsic beta-2-agonist action. Its low alpha-blocking action prevents orthostatic hypotension and improves first dose tolerance. The present study evaluates the efficacy and safety of dilevalol comparing it with captopril and nifedipine. Fifty-eight mild to moderate essential hypertensive patients were studied. After a 2 to 3 week placebo lead-in phase, patients with diastolic blood pressure between 95 and 105 mmHg were included., Patients were randomly assigned to one of the 3 study drugs for a 4-week period. Initially, 15 patients received dilevalol 200 mg qd and 15 captopril 100 mg bid; afterwards, 14 received dilevalol 200 mg qd and 14 nifedipine 40 mg bid. In the first group dilevalol decreased mean blood pressure (MBP) from 118.0 +/- 1.3 to 107.3 +/- 2.7 mmHg at week 4 and captopril from 117.8 +/- 1.2 to 108.6 +/- 2.7 (p less than 0.05). When dilevalol and nifedipine were compared, the former decreased MBP from 116.0 +/- 2.0 to 104.3 +/- 3.2 mmHg and the latter from 115.0 +/- 1.4 to 106.0 +/- 3.0 (p less than 0.05). The drug was well tolerated without evidence of orthostatic hypotension. Our results demonstrate that dilevalol is as safe and effective as captopril and nifedipine for the treatment of essential hypertension.

[Enalapril in the treatment of essential arterial hypertension]. / Enalapril en el tratamiento de la hipertensión arterial esencial.

This study evaluates the antihypertensive effects of enalapril, a new, potent, long acting angiotensin converting enzyme inhibitor. 69 patients with uncomplicated essential hypertension were included in 5 groups. Group I was used to compare the effects of enalapril and propranolol on blood pressure, renal function, plasma renin activity, aldosterone excretion and plasma lipids in 24 patients after 12 weeks. Group II was used to evaluate long term effects (48 weeks) of these drugs in 13 patients. Group III included 32 patients that received enalapril as monotherapy for 6 to 12 weeks. Group IV was studied to estimate the antihypertensive effect of low doses of hydrochlorothiazide in 18 patients receiving enalapril. Group V was used to compare the antihypertensive effect of hydrochlorothiazide, enalapril or enalapril plus hydrochlorothiazide in 19 patients. The effect on mean blood pressure was similar with enalapril and propranolol (117 versus 103 mmHg and 115 versus 104 mmHg respectively); however, glomerular filtration rate decreased with propranolol (105 versus 87 ml/min; p less than .05) and was unaltered with enalapril (102 versus 98 ml/min). Triglycerides rose with propranolol (179 versus 231 mg/dl; p less than .05) and did not change with enalapril (157 versus 121 mg/dl). In the long term, antihypertensive effects were similar and no significant side effects were observed. In 14/32 patients blood pressure became normal with enalapril alone. Low doses of hydrochlorothiazide (12.5 to 25 mg) decreased mean blood pressure by 10 mmHg when added to enalapril. The antihypertensive effect of enalapril plus hydrochlorothiazide was significant greater than that of enalapril or hydrochlorothiazide alone. Used as monotherapy, enalapril normalised blood pressure in 44% of cases. Addition of low doses of hydrochlorothiazide significantly increased the antihypertensive effect of enalapril. These results show that enalapril is a good antihypertensive agent alone or with low doses of diuretic.

Enalapril in essential hypertension.

It is now well recognised that the renin-angiotensin system plays a key role in the control of blood pressure not only through circulating angiotensin II but through its interaction with the autonomic and central nervous systems. Angiotensin-converting enzyme (ACE) inhibitors have proved to be effective in lowering blood pressure in different types of hypertension. This study evaluates the antihypertensive effects of enalapril, a new, potent, long acting ACE inhibitor. 50 patients with uncomplicated essential hypertension were included in 4 groups. Group I was used to compare the effects of enalapril and propranolol on blood pressure, renal function, plasma renin activity, aldosterone excretion and plasma lipids in 24 patients after 23 weeks. Group II was used to evaluate long term effects (48 weeks) of these drugs in 13 patients. Group III included 32 patients that received enalapril as monotherapy for 6 to 12 weeks. Group IV was studied to estimate the antihypertensive effect of low doses of hydrochlorothiazide in 18 patients receiving enalapril. The effect on mean blood pressure was similar with enalapril and propranolol (enalapril 117 versus 103 mm Hg and propranolol 115 versus 104 mm Hg); however, the glomerular filtration rate decreased with propranolol (105 versus 87 ml/min; p less than 0.05) and was unaltered with enalapril (102 versus 98 ml/min). Triglycerides rose with propranolol (179 versus 231 mg/dl; p less than 0.05) and did not change with enalapril (157 versus 121 mg/dl). In the long term, antihypertensive effects were similar and no significant side effects were observed. In 14/32 patients blood pressure became normal with enalapril alone. Low doses of hydrochlorothiazide (12.5 to 25 mg) decreased mean blood pressure by 10mm Hg when added to enalapril. The antihypertensive effect of enalapril was similar to that of propranolol; however, the lowering effect on glomerular filtration rate of propranolol did not occur with enalapril. A slight rise in triglycerides occurred only with propranolol. No significant side effects were observed with either propranolol or enalapril. Used as monotherapy, enalapril normalised blood pressure in 44% of cases. Addition of low doses of hydrochlorothiazide significantly increased the antihypertensive effect of enalapril.