BACKGROUND: Left ventricular hypertrophy is frequently noted in patients with moderate to severe chronic renal failure not requiring dialysis. Recently, several studies have shown reversal of myocardial hypertrophy in end-stage renal disease with long-term pharmacological control of blood pressure, but it is unclear whether left ventricular mass regresses or normalizes with antihypertensive treatment of patients with earlier stages of chronic renal failure. METHODS: Seventy-two undialysed patients with chronic renal failure, chronic mild-to-moderate hypertension, and left ventricular hypertrophy were randomly assigned in a prospective study to either the captopril (n = 36) or enalapril group (n = 36). Blood pressure measurements, echocardiographic and Doppler parameters were evaluated before treatment and at 6 and 12 months of therapy. RESULTS: During follow-up, six patients developed side-effects including dry cough, taste disturbances, skin rash and gastric intolerance. In the captopril group there was a decrease in mean left ventricular mass index by 12% after 6 months of treatment, which decreased by 20% after 12 months treatment. For enalapril, the average reduction of myocardial mass after 6 months treatment was 14% and after 12 months treatment, the decrease was 19%. In both treatment groups there was significant improvement of left ventricular filling dynamics. No deterioration of left ventricular systolic function was observed. CONCLUSIONS: Our results confirm that antihypertensive monotherapy with the ACE inhibitors, captopril and enalapril, in patients with chronic renal failure results in regression of left ventricular mass index associated with a significant improvement in the diastolic function of the left ventricle without a demonstrable deterioration in left ventricular systolic performance.
The authors examined 68 patients aged from 42 to 68 years with ischemic heart disease without a history of myocardial infarction and with angina pectoris of exertion functional class 2-3 and circulatory insufficiency class 2 (according to NYHA criteria). The criteria serving as the reason for relating patients to the follow-up group were left-ventricular end-diastolic volume > 160 ml, ejection fraction 0.55, threshold power of endured loads within a range of 71.5 +/- 2.30 watt. After stabilization of the clinical status by means of basic therapy (nitrates, blockers of slow calcium channels, diuretics, antiaggregants), all patients were divided into two follow-up groups. The first group consisted of 36 patients who received renitec (10 mg/24 h), patients of group 2 were given enap in the same dose. The course of treatment lasted 12 weeks. The effectiveness of treatment was controlled by echocardiography according to the standard methods in M- and B-regimens. Analysis of the obtained data showed that within 12-day follow-up renitec demonstrated higher effectiveness and lesser incidence of side-effects than did enap given in the same dose.
The combination of captopril and indomethacin has been shown to control nephrotic proteinuria in an infant with congenital nephrotic syndrome of the Finnish type. We report the satisfactory control of congenital nephrotic syndrome by enalapril, maintaining normal serum albumin levels without albumin infusions. The haplotype data of our patient were consistent with the diagnosis of a Finnish-type nephrotic syndrome. After 21 months, during which daily infusions of albumin allowed partial control of the symptoms, captopril treatment was started. No adverse effects were noted. Serum creatinine levels remained normal. Within 8 weeks, albumin infusions were completely stopped. After 1 month the treatment was changed to a single dose of enalapril (0.8 mg/kg per day). During the next 15 months, the serum protein concentration was maintained around 6.5-7 g/dl, although proteinuria persisted (0.3-0.5 g/day). Weight and length gain are now satisfactory. We conclude that enalapril may be safely used in infants with severe forms of congenital nephrotic syndrome and might allow the avoidance of aggressive treatments for prolonged periods.
OBJECTIVE--To evaluate and describe the clinical course of angio-oedema reactions induced by angiotensin converting enzyme inhibitors. DESIGN AND METHODS--All reports of angio-oedema reactions associated with angiotensin converting enzyme inhibitors submitted to Swedish Adverse Reactions Advisory Committee were reviewed and the clinical courses summarised. Numbers of cases judged to be induced by angiotensin converting enzyme inhibitors were related to their annual usage, estimated from total sales of defined daily doses, as well as to the estimated number of new patients. All cases of angio-oedema associated with angiotensin converting enzyme inhibitors reported to the World Health Organisation's international drug information system were also summarised. RESULTS--36 of the 38 reported cases in Sweden between 1981 and 1990 were judged to be related to angiotensin converting enzyme inhibitors. During 1981 through 1990, altogether 1309 cases of angio-oedema associated with angiotensin converting enzyme inhibitors were registered with the international drug information system. The incidence of reported cases of angio-oedema increased largely in parallel with the increased sales (usage) of angiotensin converting enzyme inhibitors. Of the 36 Swedish patients, 77% experienced the reaction within the first three weeks after starting treatment. 10 patients needed hospitalisation, two of whom had life threatening laryngeal obstruction. With one exception all 36 patients were free of symptoms within one week after discontinuing the drug. CONCLUSIONS--Angio-oedema induced by angiotensin converting enzyme inhibitors is a rare but potentially life threatening reaction, which in most instances occurs shortly after the start of treatment. Any patient in whom the reaction is suspected should have the treatment interrupted and, if necessary, be admitted for observation.
Comment In: BMJ. 1992 Jul 18;305(6846):1831515849
Comment In: BMJ. 1992 May 30;304(6839):14431628033
Department of Molecular and Clinical Medicine, Institute of Medicine Institute of Medicine, Section of Occupational and Environmental Medicine Institute of Medicine, Department of Public Health and Community Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg R&D Centre Primary Care, Skaraborg, Skövde Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm Centre for Bone Research at the Sahlgrenska Academy, Department of Internal Medicine and Geriatrics, University of Gothenburg, Gothenburg Karolinska Institutet, Department of Neurobiology, Care Sciences and Society, Centre for Family Medicine, Stockholm, Sweden.
Hypertension and fractures related to osteoporosis are major public health problems that often coexist. This study examined the associations between exposure to different antihypertensive drug classes and the risk of hip fracture in hypertensive patients.
We included 59?246 individuals, 50 years and older, diagnosed with hypertension during 2001-2008 in the Swedish Primary Care Cardiovascular Database. Patients were followed from 1 January 2006 (or the date of diagnosis of hypertension) until they had their first hip fracture, died, or reached the end of the study on 31 December 2012. Cox proportional hazards models were used to calculate the risk of hip fracture across types of antihypertensive medications, adjusted for age, sex, comorbidity, medications, and socioeconomic factors.
In total, 2593 hip fractures occurred. Compared to nonusers, current use of bendroflumethiazide or hydrochlorothiazide was associated with a reduced risk of hip fracture (hazard ratio 0.86; 95% CI 0.75-0.98 and hazard ratio 0.84; 95% CI 0.74-0.96, respectively), as was use of fixed drug combinations containing a thiazide (hazard ratio 0.69; 95% CI 0.57-0.83). Current use of loop diuretics was associated with an increased risk of hip fracture (hazard ratio 1.23; 95% CI 1.11-1.35). No significant associations were found between the risk of hip fracture and current exposure to beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone-receptor blockers or calcium channel blockers.
In this large observational study of hypertensive patients, the risk of hip fracture differed across users of different antihypertensive drugs, results that could have practical implications when choosing antihypertensive drug therapy.
The aim of this study was to determine whether the incidence of type 2 diabetes differed among elderly users of four major antihypertensive drug classes.
This was a retrospective, observational cohort study of previously untreated elderly patients (aged > or = 66 years) identified as new users of an antihypertensive drug class between April 1995 and March 2000. Using a Cox proportional hazards model, the primary analysis compared diabetes incidence in users of ACE inhibitors, beta-blockers, and calcium channel blockers (CCBs), with thiazide diuretics allowed as second-line therapy. In the secondary analysis, thiazide diuretics were added as a fourth study group.
In the multivariable-adjusted primary analysis (n = 76,176), neither ACE inhibitor use (hazard ratio 0.96 [95% CI 0.84-1.1]) nor beta-blocker use (0.86 [0.74-1.0]) was associated with a statistically significant difference in type 2 diabetes incidence compared with the CCB control group. In the secondary analysis (n = 100,653), compared with CCB users, type 2 diabetes incidence was not significantly different between users of ACE inhibitors (0.97 [0.83-1.1]), beta-blockers (0.84 [0.7-1.0]), or thiazide diuretics (1.0 [0.89-1.2]).
Type 2 diabetes incidence did not significantly differ among users of the major antihypertensive drug classes in this elderly, population-based administrative cohort. These results do not support the theory that different antihypertensive drug classes are relatively more or less likely to cause diabetes.
The role of atenolol in the management of patients with hypertension is currently under scrutiny. Our aim was to evaluate the real-world consequences of recent clinical trial findings.
We conducted a retrospective, cohort study using linked administrative data from the province of Saskatchewan, Canada. Eligible subjects were first-ever users of antihypertensive medications between 1 January 1994 and 31 December 2003 and were grouped into four cohorts: atenolol, angiotensin-converting enzyme inhibitors (ACEI), thiazide diuretics, or calcium antagonists. Patients remained eligible during monotherapy only.
We identified 19 249 eligible individuals (mean age 60.6 years) who were followed for a mean of 2.3 years (SD 2.0). The rate of myocardial infarction, unstable angina, stroke, or death occurred in similar frequencies among all cohorts: atenolol (2.3%), ACEI (3.6%), thiazide diuretics (2.9%), and calcium antagonists (3.9%). After adjustment for potential confounders, atenolol therapy was not associated with higher event rates than the other first-line agents, with hazard ratios ranging between 1.03 [95% confidence intervals (CI) 0.72-1.46] and 1.24 (95% CI 0.91-1.68) for all cohorts compared with atenolol. Similar results were observed upon stratifying the sample into subjects above and below 60 years of age.
The low event rates for all cohorts suggest that atenolol has not been associated with a significant burden of cardiovascular morbidity or mortality in its traditional role for uncomplicated hypertension. Further study is needed to identify the specific types of patients that should avoid atenolol as an antihypertensive agent.
Data on the national level and worldwide show a higher rate of mortality in patients with diabetes mellitus (DM) due to COVID-19, which determines the high relevance of risk factor analysis for outcomes in DM patients to substantiate the strategy for this category of patients.
To assess the effect of clinical and demographic parameters (age, gender, body mass index (BMI), glycemic control (HbA1c), and antidiabetic and antihypertensive drugs, including ACE inhibitors and ARBs) on clinical outcomes (recovery or death) in patients with type 2 DM.
A retrospective analysis of the Russian Register of Diabetes database was performed, including patients with type 2 DM (n=309) who suffered pneumonia/COVID-19 in the period from 01.02.2020 to 27.04.2020 and the indicated outcome of the disease (recovery or death) RESULTS: The percentage of lethality was determined to be 15.2% (47 of 309 people). The degree of lethality was found to be significantly higher in males (OR=2.08; 95% CI 1.1–3.9; p=0.022) and in patients on insulin therapy (OR=2.67; 95% CI; 1.42–5.02; p=0.002), while it was significantly lower in patients with an age <65 years (OR=0.34; 95% CI 0.18–0.67; p=0.001) and in patients receiving metformin (OR=0.26; 95% CI 0.14–0,5; p<0.0001), antihypertensive therapy (OR=0.43; 95% CI 0.22–0.82; p=0.009), β-blockers (OR=0.26; 95% CI 0.08–0.86; p=0.018), diuretics (OR=0.4; 95% CI 0.17–0.93; p=0.028) and renin-angiotensin system blockers (ACE inhibitors or ARBs) (OR=0.36; 95% CI 0.18–0.74; p=0.004). A tendency to an increase in lethality at higher rates of HbA1c and BMI was present, but it did not reach a statistical significance. Differences between patients receiving insulin therapy and those who were not receiving the insulin therapy were observed as follows: a significantly longer duration of type 2 DM (13.4 vs. 6.8 years, respectively; p<0.0001), worse overall glyacemic control (HbA1c: 8.1% vs. 7.0%, resp.; p<0.0001), and three times more frequent failure to achieve the HbA1c goal by more than 2.5% (14.7% vs. 5.9%, resp.; p=0.04).
The identified risk factors for lethality in patients with type 2 DM indicate that good glycemic control and previous treatment with metformin and antihypertensive drugs (including RAS blockers) could reduce the frequency of deaths. In patients on insulin therapy, a higher lethality degree was associated with worse glycemic control.
Fixed-dose combinations (FDCs) of antihypertensive agents improve therapeutic efficacy, according to current guidelines and large clinical studies.
This Russian study examined the effect on blood pressure (BP) of substituting current ineffective antihypertensive treatment with FDC perindopril/amlodipine in patients with uncontrolled hypertension.
BP was measured in the doctor's office at each visit, daily at home, and by ambulatory monitoring (ABPM) at inclusion and end-of-study.
Ninety patients (52.7 ± 12.2 years old; mean baseline BP 161.4/94.9 mmHg) at high or very high cardiovascular risk were included. FDC perindopril/amlodipine (5/5, 10/5 or 10/10 mg) exerted a rapid (2 weeks) and significant (p
Comment In: High Blood Press Cardiovasc Prev. 2015 Dec;22(4):427-826359089
BACKGROUND: The survival benefit from the use of inhibitors of angiotensin-converting enzyme (ACE) in patients with acute myocardial infarction is usually presented in terms of risk ratios and lives saved per 1000 people treated. A more relevant way to present the extent of benefit would be in terms of an increase in life expectancy, but this approach has not previously been possible because of limited data on long-term outcome. We aimed to calculate the effect of trandolapril on life expectancy with follow-up data from the Trandolapril Cardiac Evaluation (TRACE) Study. METHODS: The TRACE study previously showed a significant survival benefit with trandolapril in patients with reduced left-ventricular function after an acute myocardial infarction who were treated for at least 2 years. We ascertained the survival status of all patients in the TRACE study in June, 1998, at which time they had been followed up for a minimum of 6 years. We estimated life expectancy as median lifetime, which was the time for 50% of the patients to have died. Change in life expectancy is expressed as change in median lifetime. Analysis was by intention to treat. FINDINGS: The life expectancy of patients was 4.6 years for those given placebo versus 6.2 years for those on trandolapril. Thus, for patients on trandolapril, median lifetime was increased by 15.3 months or 27% (95% CI 7 to 51). Analysis of follow-up after the end of the study indicated no decrease of this benefit during the course of double-blind treatment; continued use of trandolapril was recommended at study closure. INTERPRETATION: In patients with severely reduced left-ventricular function, long-term treatment with an ACE inhibitor during the critical period after myocardial infarction is associated with a substantial increase in life expectancy.
Comment In: Lancet. 1999 Oct 30;354(9189):156410551537
Comment In: Lancet. 1999 Oct 9;354(9186):1301-210520662