Eur Heart J.
2005 Apr 28;
The effect of perindopril on cardiovascular morbidity and mortality
in patients with diabetes in the EUROPA study: results from the PERSUADE
substudy.
Daly CA, Fox KM, Remme WJ, Bertrand ME, Ferrari R, Simoons ML.
Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK.
AIMS: The aim of this study was to assess the effect of the angiotensin
converting enzyme inhibitor perindopril on cardiovascular events in diabetic
patients with coronary artery disease. METHODS AND RESULTS: A total of
1502 diabetic patients with known coronary artery disease and without
heart failure of 12 218 overall in the EUropean trial on Reduction Of
cardiac events with Perindopril in stable coronary Artery (EUROPA) disease
were randomized in a double-blinded manner to perindopril 8 mg once daily
or placebo. Follow-up was for a median of 4.3 years. The primary end point
was cardiovascular death, non-fatal myocardial infarction, and resuscitated
cardiac arrest. Perindopril treatment was associated with a non-significant
reduction in the primary endpoint in the diabetic population, 12.6 vs.
15.5%, relative risk reduction 19% [(95% CI, -7 to 38%), P = 0.13]. This
was of similar relative magnitude to the 20% risk reduction observed in
the main EUROPA population. CONCLUSION: Perindopril tends to reduce major
cardiovascular events in diabetic patients with coronary disease in addition
to other preventive treatments and the trend towards reduction was of
a similar relative magnitude to that observed the general population with
coronary artery disease.
Int J Clin Pract. 2005 May;59(5):600-4.
Perindopril: the reasonable choice in patients with coronary artery
disease.
Cockcroft JR.
Department of Cardiology, Wales Heart Research Institute, University
of Wales College of Medicine, Heath Park, Cardiff, UK. cockcroftjr@cf.ac.uk
Recent studies in patients with coronary artery disease (CAD) have suggested
that angiotensin-converting enzyme (ACE) inhibitors may have benefits
beyond blood pressure reduction alone. Increased arterial stiffness, itself
an emerging risk factor for CAD, adversely influences ventricular vascular
interaction, leading to an increased central aortic pulse pressure. A
number of recent studies have demonstrated a clear relationship between
central pulse pressure and angiographic CAD. Furthermore, aortic stiffness
also correlates with CAD. These studies are consistent with the hypothesis
that central aortic stiffness may promote the development of CAD and that
therapeutic intervention targeted at reducing arterial stiffness may be
of benefit in patients with CAD. The ACE inhibitor, perindopril, has been
shown to decrease arterial stiffness, largely independently of any effect
on peripheral blood pressure. Results of the recent REASON study demonstrate
that perindopril, in combination with indapamide, reduces central systolic
and pulse pressure to a greater degree than the beta-blocker atenolol
and that this effect is due to improved arterial stiffness and decreased
wave reflection. In addition to its other beneficial effects, such as
improved endothelial function and decreased inflammation, these haemodynamic
effects of perindopril may therefore have contributed to the decrease
in cardiovascular events seen in patients in the EUROPA study. Overall,
perindopril, in addition to lowering peripheral blood pressure, decreases
arterial stiffness and central pulse pressure. In individuals with CAD,
perindopril would thus appear to be a very reasonable choice.
Expert Rev Cardiovasc Ther. 2005 Jan;3(1):15-29.
Angiotensin-converting enzyme inhibition in cardiovascular disease:
evidence with perindopril.
Ferrari R.
University of Ferrara, Department of Cardiology, Arcispedale S Anna, Corso
Giovecca 203, 44100 Ferrara, Italy. fri@dns.unife.it.
Perindopril is a long-acting, once-daily lipophilic angiotensin-converting
enzyme inhibitor with high tissue angiotensin-converting enzyme affinity,
lowering angiotensinII and potentiating bradykinin. Its efficacy, safety
and tolerability are well established in the treatment of hypertension
and heart failure. Moreover, large morbidity-mortality trials, such as
the EUropean trial on Reduction Of cardiac events with Perindopril in
stable coronary Artery disease (EUROPA) and Perindopril pROtection aGainst
REcurrent Stroke Study (PROGRESS), have shown that antihypertensive treatment
with perindopril reduces and prevents cardiovascular disease in a large
range of patients with vascular diseases, whether hypertensive or not.
Thus, the outcome of these and other trials support the concept of cardiovascular
protective properties of angiotensin-converting enzyme inhibition with
perindopril in addition to the obvious blood-pressure-lowering effect.
Considering its properties and the gathered clinical evidence on efficacy
and tolerability, perindopril fulfils the criteria of the latest guidelines
for hypertension and cardiovascular disease management [1] and should
therefore be considered as a first-line antihypertensive agent, forming
a consistent part of the comprehensive strategy against hypertension and
related cardiovascular complications.
Lik Sprava. 2004 Oct-Nov;(7):34-6.
[Perindopril influence on hemostasis and functions of pancreas
in patients with ischemic heart disease]
[Article in Ukrainian]
[No authors listed]
Systemic circulation compromise in patients with cardiac insufficiency results in disturbances of functional state of pancreas. The Willebrand's Factor takes a definite role in this pathological process. The usage of Peridopril 4 mg daily during the treatment decreases significantly Willebrand's Factor activity and normalizes function of the pancreas.
Nutr Metab Cardiovasc Dis. 2004 Oct;14(5):259-69.
Effects of perindopril treatment on hemostatic function in patients
with essential hypertension in relation to angiotensin converting enzyme
(ACE) and plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms.
Jastrzebskal M, Widecka K, Naruszewicz M, Ciechanowicz A, Janczak-Bazan
A, Foltynska A, Goracy I, Chetstowski K, Wesotowska T.
Regional Center for Atherosclerosis Research, Poland. mariajas@sci.pam.szczecin.pl
BACKGROUND AND AIM: An imbalance in the hemostatic system is a frequent
finding in untreated essential hypertension (HT), and it has been shown
that treatment with angiotensin converting entyme (ACE) inhibitors improves
hemostatic function. In order to elucidate the role of genetic factors,
we studied hemostasis in patients with untreated and treated HT and correlated
the results with ACE I/D and plasminogen activator enhibitor-1 (PAI-1)
4G/5G gene polymorphisms. METHODS AND RESULTS: Forty-three males with
HT (mean age 31.7 +/- 6.8 years) were compared with 34 age and gender-matched
controls. All of the patients were treated with perindopril (4 mg/day)
and, after one and six months of therapy, their levels of plasma fibrinogen
(Fb), t-PA antigen, PAI-1 antigen, von Willebrand factor (vWF), ACE activity
and blood pressure were measured. ACE and PAI-1 genotypes were identified
by means of the polymerase chain reaction on DNA isolated from peripheral
blood lymphocytes. Untreated patients had significantly higher levels
of Fb, PAI-1 (p < 0.01) and t-PA (p < 0.05) regardless of their
ACE or PAI-1 genotypes. Perindopril reduced blood pressure regardless
of ACE or PAI-1 genotype (p < 0.001). ACE II homozygotes showed the
greatest decrease in ACE activity (p < 0.01) and a significant reduction
in Fb levels (p < 0.05) after just one month of treatment. Analysis
of the group as a whole revealed an increase in t-PA antigen levels after
six months of treatment, regardless of ACE or PAI-1 genotype (p < 0.01).
CONCLUSIONS: Our results show that essential hypertension predisposes
to the procoagulant state characterized by hyperfibrinogenemia and hypofibrinolysis.
Perindopril reduced fibrinogen levels in ACE II homozygotes due to its
more potent inhibitory action on the renin-angiotensin system in such
patients. It improved fibrinolysis by increasing t-PA levels regardless
of ACE and PAI-1 genotype.
Neurol Res. 2004 Sep;26(6):644-57.
Neuroprotective effect of the angiotensin-converting enzyme inhibitor
perindopril in MPTP-treated mice.
Kurosaki R, Muramatsu Y, Imai Y, Kato H, Araki T.
Department of Drug Metabolism and Therapeutics, Graduate School and Faculty
of Pharmaceutical Sciences, University of Tokushima, Tokushima, Japan.
The angiotensin -converting enzyme (ACE) inhibitor perindopril has been shown to exert beneficial effects on the dopaminergic system. Here, we investigated the effects of perindopril on the dopaminergic system in mice after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment, in comparison with a Ca(2+) antagonist, amlodipine. Administration of perindopril showed dose-dependent neuroprotective effects against MPTP-induced striatal dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) depletion. However, administration of amlodipine showed no significant effects on striatal dopamine depletion after MPTP treatment. In our immunohistochemical studies with antibodies against tyrosine hydroxylase (TH), microtubule-associated protein 2a, b (MAP2), dopamine transporter (DAT), parvalbumin (PV), glial fibrillary acidic protein (GFAP) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD), the administration of perindopril significantly attenuated MPTP-induced substantia nigra and striatal damage. This drug also blocked the increases in GFAP-positive astrocytes in the striatum and substantia nigra after MPTP treatment. Furthermore, the administration of perindopril showed a protective effect against the intense Cu/Zn-SOD immunoreactivity in the neurons and glial cells in both the striatum and substantia nigra after MPTP treatment. These results indicated that the ACE inhibitor perindopril can protect against MPTP-induced striatal dopamine and DOPAC depletion in mice. The protective effect may be, at least in part, caused by the reduction of free radicals caused by MPTP. The present study also demonstrated that perindopril is effective against MPTP-induced neurodegeneration of the nigro-striatal dopaminergic pathway. Furthermore, our results provided further evidence that free radical scavengers may be effective in the treatment of neurodegenerative diseases such as Parkinson's disease.
Diabet Med. 2004 Nov;21(11):1192-9.
Long-term renoprotection by perindopril or nifedipine in non-hypertensive
patients with Type 2 diabetes and microalbuminuria.
Jerums G, Allen TJ, Campbell DJ, Cooper ME, Gilbert RE, Hammond
JJ, O'Brien RC, Raffaele J, Tsalamandris C; Melbourne Diabetic Nephropathy
Study Group.
Department of Medicine, University of Melbourne, and Endocrinology Unit,
Austin Health, Studley Road, Heidelberg, 3084 Victoria, Australia. endo@austin.unimelb.edu.au
AIMS: To assess the efficacy of an angiotensin converting enzyme (ACE) inhibitor (perindopril), a dihydropyridine calcium channel blocker (sustained release nifedipine) and placebo in preventing the progression of albuminuria and decline in glomerular filtration rate (GFR) in patients with Type 2 diabetes and microalbuminaria. METHODS: A prospective, randomized, open, blinded end point study of 77 patients allocated to three treatment groups (23 perindopril, 27 nifedipine, 27 placebo). Drug doses were adjusted to achieve a decrease in diastolic blood pressure (DBP) of 5 mmHg in the first 3 months and additional therapy was given if hypertension developed (supine DBP > 90 mmHg and/or systolic blood pressure (SBP) > 140 mmHg if < or = 40 years; supine DBP > 90 mmHg and/or SBP > 160 mmHg if > 40 years). Median follow-up was 66 months, with 37 patients being followed for at least 6 years. RESULTS: Blood pressure remained within the non-hypertensive range in 83% of perindopril-, 95% of nifedipine- and 30% of placebo-treated patients (P < 0.01). In the first 12 months albumin excretion rate (AER) decreased by 47% only in the perindopril group (P = 0.04). From 12 to 72 months, AER gradients increased by 27% per year only in the placebo group (P < 0.01). After 6 years, macroalbuminuria had developed in 7/15 placebo compared with 2/11 in perindopril and 1/11 nifedipine-treated patients (P = 0.05). GFR did not change in the first 12 months, but thereafter the median GFR gradient (ml/min/1.73 m(2) per year) was -2.4 (P < 0.01) for perindopril-, -1.3 (P = 0.26) for nifedipine- and -4.2 (P = 0.01) for placebo-treated patients. The rate of decline in GFR for the study group as a whole from 12 months to the end of follow-up correlated negatively with mean arterial pressure (MAP) (r = -0.38, P < 0.01). During a 3-month treatment pause in 29 patients AER tended to increase only in the perindopril group (P < 0.07). CONCLUSIONS: Long-term control of blood pressure with perindopril or nifedipine stabilizes AER and attenuates GFR decline in proportion to MAP in non-hypertensive patients with Type 2 diabetes and microalbuminuria.
Stroke. 2004 Sep;35(9):2117-22. Epub 2004 Jul 15.
Long-term angiotensin-converting enzyme inhibitor perindopril
therapy improves cerebral perfusion reserve in patients with previous
minor stroke.
Hatazawa J, Shimosegawa E, Osaki Y, Ibaraki M, Oku N, Hasegawa
S, Nagata K, Hirata Y, Miura Y.
Department of Radiology, Research Institute of Brain and Blood Vessels,
Akita, Japan. hatazawa@tracer.med.osaka-u.ac.jp
BACKGROUND AND PURPOSE: Angiotensin-converting enzyme (ACE) inhibitor-based therapy reduces the recurrence of stroke. The present study assessed the effects of long-term ACE inhibitor therapy on cerebral circulation in patients with previous minor stroke. METHODS: After a run-in period, 19 patients were randomized to ACE inhibitor therapy (n=9; 4 mg of perindopril daily; mean age, 64+/-8 years; mean systolic/diastolic blood pressure [BP]+/-SD, 133+/-12/77+/-9 mm Hg) or placebo therapy (n=10; mean age, 66+/-9 years; mean BP, 139+/-10/78+/-8 mm Hg). Cerebral blood flow (CBF) was measured during hypercapnia, normocapnia, and hypocapnia using a positron emission tomography with H2(15)O at entry into the study and after 3 to 12 months. Cerebral perfusion reserve (CPR) was defined as percent CBF response to a 1 mm Hg change in arterial partial pressure of CO2 between hypercapnia and hypocapnia. RESULTS: Systolic/diastolic BP and CBF during normocapnia showed no significant changes between entry and completion of the trial in the perindopril and placebo groups. Mean value of CPR showed a significant increase in the perindopril group (from 3.7+/-1.7%/mm Hg to 4.8+/-1.7%/mm Hg; P<0.05) but not in the placebo group (from 4.1+/-0.8%/mm Hg to 4.2+/-0.6%/mm Hg; NS). Statistical parametric mapping analysis also showed global and significant increase (P<0.01, uncorrected) in CPR in the perindopril group alone. CONCLUSIONS: Long-term ACE inhibitor-based therapy had a beneficial effect on the cerebral circulation by improving CPR in patients with previous minor stroke.
Can J Cardiol. 2004 Jun;20(8):795-9.
Effects of perindopril on elastic and structural properties of
large arteries in essential hypertension.
Lacourciere Y, Beliveau R, Conter HS, Burgess ED, Lepage S, Pesant
Y, Spence JD, Asmar R, Carriere S, Plante GE; Canadian Hypertension Society.
Centre Hospitalier de l'Universite Laval, Sainte-Foy, Quebec. yves.lacourciere@crchul.ulaval.ca
BACKGROUND: Perindopril, an angiotensin-converting enzyme (ACE) inhibitor, is a well-recognized antihypertensive drug. Its ability to protect against cardiovascular events in hypertension has also been demonstrated. It decreases the stiffness of the larger arteries; questions remain as to the mechanisms involved and whether it is blood pressure (BP) control-dependent. OBJECTIVES: To correlate the BP response to ACE inhibition therapy with changes in arterial stiffness as evaluated by pulse wave velocity (PWV), and to correlate these changes in arterial stiffness with alterations in indicators of vascular collagen metabolism serum levels of metalloproteinase (MMP)-1 and tissue inhibitor of MMP-1 (TIMP-1). METHODS: A total of 162 patients aged 18 to 70 years with stage 1 and 2 essential hypertension (diastolic BP 95 mmHg to 114 mmHg) were enrolled to receive six months (M6) of therapy with the ACE inhibitor, perindopril. Patients were either treatment-naive or had not received any antihypertensive treatment for at least six months before the study. RESULTS: Mean BP was significantly reduced after two months (M2) of therapy (P=0.00001) and remained stable thereafter. In addition to the significant mean changes in PWV observed at M2 (P=0.00001), further reductions in PWV were noted at M6 (P=0.007). The change in PWV between baseline (M0) and M2 was significantly correlated to all BP parameters at M0 (correlation coefficient at M2 was 0.189 or greater). However, no correlation was seen regarding BP parameters at M2 and further M2 to M6 changes in PWV, suggesting a decrease of arterial stiffness independent of BP reduction. The expression of TIMP-1 and MMP-1 was highly variable and demonstrated no correlation with BP or PWV. CONCLUSIONS: Reductions in BP and PWV appear to be correlated during the first two months of perindopril therapy. After six months, PWV continues to decrease independently of any further reduction in BP, suggesting the occurrence of a pressure-independent pharmacological remodelling of the arterial wall. A long-term, double-blind, randomized trial could be required to confirm that the observed increase in vascular distensibility induced by perindopril is related to a mechanism of action other than a reduction in BP.
Stroke. 2004 Aug;35(8):1899-902. Epub 2004 May 27.
Effect of perindopril on cerebral vasomotor reactivity in patients
with lacunar infarction.
Walters M, Muir S, Shah I, Lees K.
Gardiner Institute, Western Infirmary, Division of Cardiovascular and
Medical Sciences, University Department of Medicine and Therapeutics,
University of Glasgow, Glasgow, Scotland. m.walters@clinmed.gla.ac.uk
BACKGROUND AND PURPOSE: There is growing evidence that pharmacologic interference with the renin-angiotensin system may reduce risk of stroke, although the mechanism is unclear. Impaired reactivity of cerebral vessels has recently been recognized as a risk factor for stroke. We examined the effect of the angiotensin-converting enzyme (ACE) inhibitor perindopril on cerebral vasomotor reactivity to acetazolamide in patients with lacunar cerebral infarction. METHODS: We studied a cohort of male patients between 3 and 12 months after lacunar infarction confirmed on computed tomography. Each patient received perindopril 4 mg daily or matching placebo for 2 weeks in a randomized, double-blind, placebo-controlled crossover fashion. A 1-week washout period was observed between dosing periods. Cerebral vasomotor reactivity (increase in middle cerebral artery mean flow velocity in response to intravenous injection of 15 mg/kg acetazolamide) was measured before and after each dosing period using standard Doppler ultrasound techniques. RESULTS: Twelve patients (mean age 63.2+/-2.3 years) completed the protocol. There was no treatment order effect. Cerebral vasomotor reactivity was significantly greater after perindopril treatment (percent change from baseline +18.8+/-10.1% after perindopril, -4.6+/-4.1% after placebo; P=0.032). Dosing with perindopril did not affect resting cerebral blood flow velocity (percent change from baseline +3.1+/-9.5% after perindopril, -0.6+/-5.4% after placebo), nor was there a change in resting blood pressure (+1.8 mm Hg+/-3.1 after perindopril, +1.4 mm Hg+/-2.5 after placebo). CONCLUSIONS: This study provides evidence of a significant improvement in cerebral vasomotor reactivity induced by perindopril, beyond any effect on blood pressure. The results suggest a possible mechanism for the beneficial effect of ACE inhibition on stroke risk observed in recent clinical trials, and suggest a role for the renin-angiotensin axis in the pathophysiology of subcortical small vessel disease.
Am J Ther. 2004 May-Jun;11(3):199-205.
Clinical experience with perindopril in patients nonresponsive
to previous antihypertensive therapy: a large US community trial.
Guo W, Turlapaty P, Shen Y, Dong V, Batchelor A, Barlow D, Lagast
H.
Clinical Operations and Medical Affairs, Solvay Pharmaceuticals Inc.,
Marietta, Georgia 30062, USA.
A subgroup analysis of a large US community trial was conducted to evaluate the antihypertensive efficacy and safety of perindopril, an angiotensin-converting enzyme inhibitor (ACEI), in 3159 patients who lacked blood pressure (BP) control at entry with previous antihypertensive therapy. Patients received 4 mg perindopril daily for 6 weeks. Based on physicians' assessment of BP response, the patients were then either maintained on 4 mg daily (group 1) or the dose was increased to 8 mg daily (group 2) for an additional 6 weeks. The mean baseline sitting BP was 158.2/92.9 mm Hg. Perindopril monotherapy produced a significant BP decrease from baseline of 11.6/6.5 mm Hg and 14.9/8.4 mm Hg at weeks 6 and 12, respectively. In group 1 patients, the majority of BP decrease occurred at week 6 (17.3/9.5 mm Hg) and was maintained until the end of week 12 (18.2/10.1 mm Hg). In group 2 patients, the BP decrease on the 4-mg dose was modest at week 6 by 5.2/3.1 mm Hg. However, further dose up-titration of perindopril to 8 mg resulted in a clinically significant BP decrease of 11.9/6.8 mm Hg from baseline to week 12. Significant antihypertensive effects of perindopril were also demonstrated in the special patient populations of elderly (>or=65 years), black, isolated systolic hypertension, patients with concomitant cardiovascular diseases, and patients nonresponsive to other ACEI therapy. Overall, BP control (<140/<90 mm Hg) was achieved in 40.0% of patients at week 12. Perindopril was well tolerated with cough and angioedema reported in 8.5% and 0.4% patients, respectively. Physicians assessed therapeutic response to perindopril as satisfactory in 73.8% patients who were nonresponsive to previous antihypertensive therapy. These results suggest that, in a community-based practice, perindopril monotherapy (4-8 mg/d) is an effective and safe therapeutic option in patients nonresponsive to previous antihypertensive therapy.
Curr Hypertens Rep. 2004 Jun;6(3):201-7.
Prevention of dementia and cerebroprotection with antihypertensive
drugs.
Hanon O, Seux ML, Lenoir H, Rigaud AS, Forette F.
Hopital Broca, CHU Cochin Port-Royal, Universite Rene Descartes, Paris
V, 54/56 Rue Pascal, 75013 Paris, France. olivier.hanon@brc.ap-hop-paris.fr
High blood pressure is a major risk factor for stroke and is also closely correlated with cognitive decline and dementia. Indeed, most longitudinal studies showed that cognitive functioning is often inversely proportional to blood pressure values measured 15 or 20 years previously. Because of the aging of the population, the frequency of stroke and dementia will dramatically increase in the coming years. Therefore, the prevention of cerebrovascular and cognitive disorders represents a major challenge. Antihypertensive drugs have shown clinical benefits in both primary and secondary prevention of strokes. Consensus is generally that blood-pressure lowering represents the major determinant of the benefit conferred by the antihypertensive treatment for stroke prevention; however, recent studies have suggested some differences between classes of antihypertensive drugs. The results of therapeutic trials (Systolic Hypertension in Europe, Perindopril Protection Against Recurrent Stroke Study [PROGRESS]) open the way to the prevention of dementia (vascular or Alzheimer's type) by antihypertensive treatments. These two studies suggest different mechanisms for the prevention of cognitive decline using antihypertensive drugs. In this context, reduced incidence of dementia should be the primary outcome of future trials comparing different classes of antihypertensive drugs.
Hypertens Res. 2004 Mar;27(3):147-56.
Effects of perindopril-based blood pressure lowering and of patient
characteristics on the progression of silent brain infarct: the Perindopril
Protection against Recurrent Stroke Study (PROGRESS) CT Substudy in Japan.
Hasegawa Y, Yamaguchi T, Omae T, Woodward M, Chalmers J; PROGRESS
CT Substudy Investigators.
Cerebrovascular Division, National Cardiovascular Center, 5-7-1, Fujishirodai,
Suita 565-8565, Japan. yazhaseg@hsp.ncvc.go.jp
Controversy persists as to whether reducing the blood pressure of patients with a history of stroke leads to an increased risk of silent brain infarct (SBI) and dementia. A total of 667 patients were randomized to receive the angiotensin-converting enzyme (ACE) inhibitor perindopril (4 mg daily), with or without the diuretic indapamide (2 mg daily) or matching placebo(s). Brain CT scanning was performed annually over the mean follow-up period of 3.9 years. Active treatment reduced the blood pressure (systolic/diastolic) by 5.2/2.6 mmHg over the follow-up period. A total of 119 new SBI were detected and 92% of them were lacunar type small infarcts. The frequency of reaching the primary end-point (recurrent symptomatic stroke or new SBI) was similar in the placebo group (26.5%) and in the active treatment group (25.9%). There was no significant difference in brain atrophy indices between two groups. In the subgroup with a history of large artery infarction, 7 out of 55 patients from the placebo group developed new SBI, while none of the 40 patients from the active treatment group did so (p = 0.020). The baseline diastolic blood pressure was significantly associated with the risk of new SBI (p = 0.004), but the stroke subtype was not. In conclusion, blood pressure-lowering with a perindopril-based regimen did not increase the risk of SBI and brain atrophy in patients with a history of stroke. The baseline diastolic blood pressure was an independent predictor of new SBI, but the index stroke subtype did not influence the risk of SBI.
Curr Cardiol Rep. 2004 Mar;6(2):124-9.
Treatment of hypertension and prevention of ischemic stroke.
Aronow WS, Frishman WH.
Department of Medicine, New York Medical College, Munger Pavilion, Room
263, Valhalla, NY 10595, USA.
Data clearly indicate that treatment with antihypertensive drugs reduces the incidence of all strokes in men (by 34%), women (by 38%), elderly persons (by 36%), including those older than 80 years (by 34%), younger persons, those with systolic and diastolic hypertension, persons with isolated systolic hypertension, and in those with a history of stroke or transient ischemic attack (by 28%). Blood pressure should be reduced to less than 140/90 mm Hg. The overall data also suggest that reduction of stroke in persons with hypertension is related more to a reduction in blood pressure than to the type of antihypertensive drugs used.
Am J Hypertens. 2004 Jan;17(1):14-20.
Perindopril effects on ambulatory blood pressure: relation to
sympathetic nervous activity in subjects with diabetic nephropathy.
Yasuda G, Hasegawa K, Kuji T, Ogawa N, Shimura G, Umemura S,
Tochikubo O.
Division of Nephrology, Yokohama City University School of Medicine, Kanagawa,
Japan. y911429@urahp.yokohama-cu.ac.jp
BACKGROUND: Few studies have reported the effect of angiotensin-converting enzyme inhibitors on 24-h blood pressure (BP) and regulation of sympathetic nervous activity in hypertensive patients with diabetic nephropathy. Using ambulatory BP monitoring (ABPM) devices equipped with spectral analysis of heart rate variability, we assessed the effects of perindopril on 24-h BP and autonomic nervous activity in these patients. METHODS: Thirty-four hypertensive patients with non-insulin-dependent diabetic nephropathy underwent ABPM before and after treatment with perindopril (final dose: 4.9 +/- 1.8 mg/d). Simultaneously, spectral analysis was performed to calculate the high frequency components (HF) as a marker of parasympathetic nervous activity, and the low frequency components (LF)/HF ratios as an index of the sympathovagal balance. RESULTS: Perindopril significantly and equally decreased the waking and sleeping BP in the diabetic patients. During the sleeping period, the magnitude of change of mean BP induced by perindopril correlated inversely with the sleeping/waking ratio of mean BP before treatment. However, there was no correlation between these parameters during the waking period. Perindopril decreased both waking and sleeping LF/HF ratios, although no differences in HF components were observed between before and after treatment. CONCLUSIONS: In patients with diabetic nephropathy, perindopril decreased 24-h BP. Spectral analysis suggested that this finding was partially related to inhibited sympathetic nervous activity. During sleeping periods, the BP-lowering effect of perindopril was more pronounced in patients showing no nocturnal decrease in BP. Perindopril may be a potent antihypertensive agent to reduce increased nocturnal BP, a risk factor of target organ damage in these patients.
