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The efficacy and tolerability of long-term treatment with the angiotensin converting enzyme inhibitor captopril was evaluated in elderly hypertensive subjects. One hundred thirty patients were studied (61 men and 69 women; mean age, 68.33 ± 5.49 years), all with mild to moderate arterial hypertension (mild = 90–105 mmHg; moderate = 105–115 mmHg). Patients with secondary hypertension were excluded from the study. After a 2-week drug washout, patients were given captopril 25 to 100 mg/day alone or in combination with hydrochlorothiazide (HCTZ) 25 mg/day for 15 weeks. After 2 weeks of treatment, significant decreases in systolic and diastolic blood pressures were observed (P

The aim of this study was to evaluate the pathophysiological role of fibrinogen in patients with chronic or acute ischemic coronary syndromes on the basis of epidemiological and clinical evidences showing the importance of fibrinogen as a risk factor for cardiovascular diseases and atherosclerosis progression.We evaluated the behavior of plasma fibrinogen in 310 hospitalized patients with 1) acute myocardial infarction (n = 98); 2) unstable angina (n = 87); 3) chronic ischemic heart disease (n = 75); and 4) in controls without myocardial ischemia (n = 50). Fibrinogen was evaluated, by using the Clauss method, on day 1 and 5 during in hospital-stay and at 6-month follow-up in patients suffering from acute myocardial infarction.Plasma levels of fibrinogen were higher in patients with chronic ischemic heart disease (335.3 +/- 81.2 mg/dl, p0.001) and especially in patients with acute myocardial infarction (454.72 +/- 69.5 mg/dl, p0.00001) and unstable angina (382.6 +/- 101.3 mg/dl, p0.00025) in comparison with controls (271.28 +/- 62.4 mg/dl). Q wave myocardial infarction showed higher levels of fibrinogen than non-Q wave (461.3 +/- 95.8 vs 422.5 +/- 71.3 mg/dl, p0.02). Patients with acute myocardial infarction showed a further increase in fibrinogen on day 5 in comparison with entry levels (525.88 +/- 87.3 vs 454.7 +/- 69.5 mg/dl, p0.00001) regardless of the fibrinolytic treatment. Patients who died (n = 6) or had severe arrhythmias (n = 4) during in-hospital stay as well as those with post-infarction angina (n = 20) showed higher fibrinogen levels.Our results confirm the role of fibrinogen as a risk factor for ischemic heart disease, especially in patients with unstable angina and acute myocardial infarction. In the latter, elevated fibrinogen values seem also to be associated with a worsen prognosis during hospitalization.

To evaluate the behavior of cardiac arrhythmias (CA) and transient episodes of myocardial ischemia (TEMI), in relation to the circadian pattern of blood pressure in patients suffering from arterial hypertension, with or without echocardiographically ascertained left ventricular hypertrophy (LVH), we studied 128 patients, 87 men (M) and 41 women (F), aging from 21 to 76 years, subdivided into two groups: Group I, including 66 patients with LVH (45 M and 21 F; mean age of 53.7 ± 9.1 years; Group II, including 62 patients without LVH ( 42 M and 20 F; mean age of 49.7 ± 9.5 years). Office blood pressure (OBP) as well as nighttime ambulatory blood pressure (ABP) were higher in patients with LVH (P < .05 and P < .01). CA were present in a higher number of patients of Group I (P < .001): premature supraventricular beats (PSVB) 22.7 v 4.8%, supraventricular couplets (SVC) 36.4 v 16.1%, supraventricular tachycardia runs (SVT runs) 27.3 v 12.9%, ventricular ectopic beats (VEB) 25.6 v 8.0%, ventricular couplets (VC) 30.3 v 12.9%, ventricular tachycardia runs (VT runs) 12.1 v 3.2%. The absolute number of ectopic beats was also significantly higher in patients of Group I. Ventricular arrhythmias were significantly related to ASBP (r = 0.83, P < .01), to ADBP (r = 0.74, P < .01) and to heart rate (r = 0.87, P < .01) in patients of Group I. TEMI were more frequent in patients of Group I (73 v 41 episodes, 39.39% v 25.8% of patients, P < .01) and were related to ABP peaks. In fact, in both groups of patients all TEMI without heart rate increase and most TEMI with heart rate increase were registered between 6:00 and midnight, hours in which ABP values were higher. We conclude that hypertensives with LVH, but without clinical history of coronary heart disease, have a higher prevalence of ventricular arrhythmias and of transient episodes of myocardial ischemia in relation to the circadian pattern of ABP.

The aim of our study was to evaluate the behaviour of venous pressure in patients with systodiastolic arterial hypertension as compared with elderly patients suffering from isolated systolic hypertension and with healthy controls. We studied 125 subjects subdivided into three groups: Group A, formed by 32 patients, aged between 43 and 73 years, with a mean age of 63.25+/-12.3 years, suffering from mild to moderate systodiastolic essential arterial hypertension (SDH); Group B, including 50 patients, aged between 58 and 83 years, with a mean age of 71.53+/-8.43 years, with isolated systolic hypertension (ISH); Group C, formed by 43 subjects, aged between 13 and 72 years, with a mean age of 42.91+/-17.84 years, as a healthy control group (CS). Patients observed a period of pharmacological washout for at least 15 days before the beginning of the study. All underwent a diet with a normal sodium intake. Brachial arterial pressure was always measured at 9 a.m., by using a mercury sphygmomanometer. The venous pressure was measured at the fold of the elbow on the basilic vein, using a Doppler ultrasound instrument. The SBP was similar in patients with SDH (Group A) and in those with ISH (Group B); in both groups SBP was significantly higher than in CS (Group C) (p0.001). The DBP was significantly higher especially in patients of group A, but also in patients of group B, in comparison with subjects of group C and in patients with SDH in comparison with those with ISH. Venous pressure (VP) proved to be significantly higher in both groups of hypertensives in comparison with CS and in SDH in comparison with ISH (14.76+/-1.90 in Group A vs 12.53+/-2.39 in group B vs 8.75+/-2.02 mmHg in group C, p0.0001). Considering ten subjects, matched for sex and age in each group, we observed again that VP values in SDH wereISHCS (14.3+/-2.9 vs 9.7-/+1.8 in SDH vs CS, 13.5-/+2.1 vs 10.7+/-1.9 in ISH vs CS, 15.6+/-2.2 vs 11.6+/-2.6 mm Hg in SDH vs ISH, p0.001). In all three considered groups a significant correlation between the values of SBP and DBP with VP (p0.001) was observed. In conclusion, data from our study show that hypertension is a disease in which both the arterial and the venous vascular beds are involved with increased pressure in both circulatory beds.

Twenty four male hypertensive patients suffering also from peripheral obstructive arterial disease were randomly subdivided in two groups and after a period of farmacological wash-out of one month Group I was treated with Captopril (C 50 mg bid) or Ticlopidine (T 250 mg bid) for three months and then with the association C plus T for three months again. After placebo administration for one month, patients were further treated with C plus T at low doses (25 mg bid and respectively 250 mg daily). In the first part of the study, patients of Group II received an inverse sequence of the drugs (before Ticlopidine 250 mg bid and then Captopril 50 bid). In both groups of patients C induced a significant decrease of blood pressure and an increase of PFWD, TWD, and WI. T did not modify blood pressure but slightly increased PFWD, TWD, and WI. The improvement was more evident during administration of C plus T, whereas placebo administration induced a trend toward baseline values. Finally, the chronic administration of C plus T for twelve months induced a further improvement of all considered parameters. In conclusion, chronic administration of C plus T may be useful in the treatment of hypertensive patients suffering from intermittent claudication, improving significantly PFWD and TWD.

Silent myocardial ischemia (SMI) has been demonstrated in 2 to 5% of subjects in totally asymptomatic population, in 30% of patients with history of previous myocardial infarction and in 60 to 100% of patients with stable or unstable angina pectoris. In these patients, 60 to 80% of transient episodes of ischemia are silent and SMI is induced by daily activities and so can be registered during continuous ECG monitoring. The finding of SMI during an exercise testing or during ambulatory monitoring has an unfavourable prognostic significance both in apparently asymptomatic subjects and in patients suffering from stable or unstable angina pectoris or survivors to a myocardial infarction. Stress testing and Holter monitoring are the most used non invasive tests to detect SMI. The sensitivity and specificity of ergometer test can be improved by 201-Tl myocardial scintigraphy. Moreover, the ergometer test can be used as a provocative test to induce changes in regional wall kinesis and so these alterations can be evaluated by using echocardiogram and radioisotopic or contrast ventriculography. The echocardiogram allows to evaluate the presence of kinesis changes induced by stress test or by pharmacological stimulation with dipyridamole or dobutamine. SMI can be also detected through the study of metabolic alterations during cardiac catheterism.

Aim of this study has been to evaluate the prevalence of arterial hypertension and other risk factors in patients suffering with PAD in two clinical samples (1.: 102 patients with PAD, 69 M, 33 F, studied in our angiology laboratory, matched for sex and age with 102 healthy volunteers; 2.: 184 hospitalized patients, 80 M, 104 F, mean age 57.2 +/- 10.8, with PAD) and in two epidemiological studies (1.: Trabia Study, 835 subjects; and 2.: Casteldaccia Study, 723 subjects). All patients performed a full clinical and laboratory examination, including the determination of the ankle/arm pressure ratio (Winsor index, positive for PAD when lower than 0.95). In the first clinical study we observed a significantly (p0.01) greater prevalence of arterial hypertension (51.9 vs 9.8%), hypercholesterolemia (48.2 vs 21.6%), hypertriglyceridemia (53.7 vs 26.1%), smoking habit (64.3 vs 44.2%), and hyperglycemia (26 vs 7.9%) in PAD patients than in controls. In the second clinical study, considering separately the patients under and over 65 years, all risk factors resulted more prevalent in younger people than in the aged, except diabetes and hypertension.

The aim of this study was to evaluate the prevalence of arterial hypertension and other risk factors in patients suffering from peripheral arterial disease (PAD) in two clinical samples (1.: 102 patients with PAD 69 M, 33 F, studied in our angiology laboratory, matched for sex and age with 102 healthy volunteers; 2.: 184 hospitalized patients, 80 M, 104 F, mean age 57.2 +/- 10.8, with PAD) and in two epidemiological cohorts (1.: Trabia Study, 835 subjects; 2.: Casteldaccia Study, 723 subjects). All patients were subjected to a full clinical and laboratory examination, including the determination of the ankle/arm pressure ratio (Winsor index, positive for PAD when lower than 0.95). In the first clinical study we observed a significantly (p0.01) greater prevalence of arterial hypertension (51.9 vs 9.8%), hypercholesterolemia (48.2 vs 21.6%), hypertriglyceridemia (53.7 vs 26.1%), smoking habit (64.3 vs 44.2%), and hyperglycemia (26 vs 7,9%) in PAD patients than in controls. In the second clinical study considering separately the patients under and over 65 years, all risk factors resulted to be more prevalent in younger people than in the aged, except for diabetes and hypertension. In our epidemiological experience, the prevalence of PAD increases with aging, above all in males. In the Trabia Study the risk factors, more associated with PAD, were hypercholesterolemia, smoking and obesity (41.18%) in males and hypertension and hypercholesterolemia (33.3%) and obesity (25%) in females. In the Casteldaccia Study the most important risk factors were smoking (64.28%), hypercholesterolemia (42.86%) and hypertriglyceridemia (35.71%) in males, and obesity (60%), hypercholesterolemia (30%) and diabetes (20%) in females. Cholesterol levels and smoking were significantly higher in PAD patients than in the general population, whereas hypertriglyceridemia and glycemia were not. Arterial hypertension was significantly associated with PAD in the Trabia but not in the Casteldaccia Study. Obesity was significantly associated to PAD in females in both studies. In the Casteldaccia Study, lower HDL-cholesterol levels were observed in PAD patients, above all in males, whereas significantly greater Apo-B values and lower Apo-A1 levels (in males) were shown. The different levels of associated risk factors and their prevalence in PAD patients confirm the multifactorial pathogenesis of atherosclerosis. The exact role of each risk factor in the genesis of PAD is difficult to be evaluated due to the complex biological and statistical interrelationships among different risk factors. However, the management of associated risk factors may favourably influence the risk profile in each patient suffering from PAD.

We studied the structural and functional characteristics of the vascular bed at calf level in 46 middle aged hypertensive patients (20 males and 26 females) treated with different beta-blockers. After one week of placebo, the patients were divided into three groups: group 1 was treated with labetalol, an alpha-beta-blocker (200 mg t.t.d.); group 2 was treated with acebutolol, a cardioselective beta-blocker with intrinsic sympathomimetic activity (ISA) (200 mg t.t.d.); group 2 was treated with acebutolol, a cardioselective beta-blocker with intrinsic sympathomimetic activity (ISA) (200 mg t.t.d.); group 3 was treated with metoprolol, a cardioselective beta-blocker without ISA (100 mg t.t.d.). Before and after placebo, and after three months of active drug treatment, we measured blood pressure, and rest and peak flow at the calf level by strain gauge plethysmography. Basal and minimal vascular resistances were calculated as the ratio between mean blood pressure and rest or peak flow, respectively. A significant decrease in blood pressure was observed in each group. However, basal and minimal vascular resistances decreased only in the labetalol-treated group. These observations indicate that antihypertensive agents that have similar effects on blood pressure, may have different effects on minimal vascular resistance. Therefore, maximum vasodilation of arterioles improves, suggesting that long term treatment with labetalol, but not with other beta-blockers is able to induce a partial regression of vascular structural alterations in hypertensive patients.

Arterial hypertension is a definite risk factor for the atherosclerotic disease and thus has a primary role in the genesis of cardiovascular diseases, but it acts also though a direct structural damage of great and small arteries and arterioles. Up to date, clinical research and technological advancements have made possible the development of instruments and methods for the evaluation of the vascular damage. Ultrasonographic methods are now the better non invasive tools for the study of arterial diseases, allowing a definition power comparable to angiography, and giving useful data on characters and composition of plaques, also minimal, at the level of the arterial district of lower limbs, epiaortic, renal, and abdominal vessels. These methods allow the study of the vascular lesion under the hemodynamic (CW or pulsed Doppler with spectral signal analysis) and the morphological profile (high resolution echotomography) or both echo-Doppler duplex scanning or color flow imaging). Arterial compliance of great vessels can be studied through the Doppler evaluation of pulsed wave velocity along the arterial tree. Other useful parameters are the aortic distensibility (ratio between % change in arterial volume and blood pressure), the elastic module, the index of arterial rigidity and the aortic index (ratio between pulse pressure and stroke volume). By using this latter parameter we demonstrated a significant decrease of arterial compliance that is proportional to the severity of blood pressure values. Small vessels may be studied through strain-gauge plethysmography, that allows to obtain the regional blood flows at the hand and forearm (skin circulation) and the calf (muscular circulation) both in basal conditions and after ischaemic stimulus. From the ratio between mean arterial pressure and post-ischemic blood flow it is possible to obtain minimal vascular resistances, expression of the maximal vasodilatation capacity in the arteriolar bed. With this method we showed that minimal vascular resistances increase proportionally with the increase of blood pressure in borderline hypertensives, in mild, moderate and severe stable arterial hypertension and in hypertension of the aged. The cutaneous microcirculation may be studied also by laser Doppler and capillaroscopy, that show a reduced capillary perfusion in hypertension. Clinically, these diagnostic tools are also extremely useful for studying the effects of antihypertensive treatment on structure and function of arterial vessels, as it seems that some drugs are able to counteract the structural alterations related to hypertension.

Arterial hypertension is often complicated by left ventricular hypertrophy (LVH) and by vascular structural changes resulting in decreased proximal and distal compliance. LVH is an adverse prognostic factor because it increases the incidence of sudden death and other morbid events related to ischaemic heart disease, whereas vascular alterations may induce target organ damage and contribute to the maintenance of elevated blood pressure values. Thus, antihypertensive treatment must both reduce blood pressure and halt regression of cardiovascular structural changes. A review of the literature suggests long-term use of calcium antagonists, ACE inhibitors, and beta-blockers may revert LVH. We have found that such long-term drug use not only reduces blood pressure and LVH, but also ventricular arrhythmias that are often related to cardiac hypertrophy; however, diuretics do not have this beneficial effect. As regards vascular disturbances ACE inhibitors partially revert these alterations, whereas beta-blockers do not. Further studies are needed to determine whether there are regional differences in the regression of cardiovascular structural changes or whether different antihypertensive drugs have different effects on these changes.

The aim of this study was to evaluate the effects of the transdermal application of nitroglycerin (NGT) on exercise tolerated and regional myocardial perfusion, as evaluated by 201 thallium stress scintigraphy, in patients with stable effort angina. We studied 20 patients, 15 men and 5 women, aged between 43 and 68 years, with average age of 55 +/- 8 years, suffering from effort angina, whose angina threshold was stable in 3 stress testing performed in the week before the study started. The patients, after a pharmacological washout of 1 week, underwent 2 exercise testing 20 hours after the application of a patch containing placebo or 10 mg NGT, with an interval of 7 days. 60-90 s before stress testing was interrupted, 2 mCi of thallium 201 were injected in an antecubital vein of the arm. The scintigraphic images were obtained soon in the 0, 45 and 90 degree views and after 4 hours reperfusion. Under placebo patch all patients interrupted ergometer test for angina, while under the patch containing active NGT angina was present in 11/20 patients and 9 patients stopped the test because of muscular exhaustion. NGT induced an increase of the ergometer test duration (+26%); this difference was statistically significant. The ST segment downsloping decreased significantly both at maximal common work and at exercise peak after NGT application in comparison with placebo. The perfusional defects observed on the scintigraphic images obtained soon after the exercise (and reversible after 4 hours of reperfusion) on placebo patch, diminished significantly after NGT and the captation index lung/heart decreased also significantly (from 49 to 41%), showing so an improvement of cardiac performance. In conclusion the transdermal application of NGT, in patients with effort angina, demonstrated to have antianginal and antiischemic effect, reducing the number of patients interrupting the stress testing for angina, increasing the exercise tolerated and diminishing the ST segment downsloping, objective demonstration of myocardial ischemia. This antianginal and antiischemic effect might follow to the reduction of the preload induced by nitrates, in part also the reduction of the afterload, factors determining a decrease of the wall tension and so of MVO2, but also to a redistribution of the subendocardial flow as demonstrated by 201-Tl scintigraphic images. These effects induce also a global improvement of the left ventricular function as demonstrated by the reduction of the lung/heart index of thallium captation.

Ketanserin is a new potent antiserotonergic drug which, unlike previous ones, is selective for S2-serotoninergic receptors and does not have an agonist action. A trial was carried out on medium-term treatment with ketanserin or propranolol in subjects suffering from mild to moderate hypertension. The trial was designed as a double-blind crossover randomized study comparing either ketanserin or propranolol with placebo. Thirteen patients completed the study, which was divided into two groups (A and B). Systolic (SBP), diastolic (DBP) and mean (MBP) blood pressures were measured by non-invasive, intermittent ambulatory monitoring performed using a Pressurometer II, from Del Mar Avionics. Heart rate was measured using a continuous electrocardiogram monitoring. Systolic blood pressure was significantly reduced both after ketanserin (A:11.1%; B:10.8%) and propranolol (A:11.7%; B:11.8%) but in group A its decrease was more pronounced after propranolol (P less than 0.01). Diastolic blood pressure was significantly reduced both after ketanserin (A:11.5%; B:11.1%) and propranolol (A:11.4%; B:11.9%), as was MBP (A:11.9%; B:11.8% for ketanserin and A:11.9%; B:11.9% for propranolol). The heart rate diminished significantly only after propranolol administration (P less than 0.01). Ambulatory monitoring showed a significant 24-h reduction of SBP after administration of propranolol (P less than 0.0025) and ketanserin (A:P less than 0.0025, B: P less than 0.005). Diastolic blood pressure was also significantly reduced after ketanserin (P less than 0.0005) and propranolol (A: P less than 0.0025, B: P less than 0.0005). The heart rate obtained by continuous electrocardiogram monitoring diminished significantly only after propranolol administration (P less than 0.0005). No significant changes of circadian behaviour of blood pressure were observed.

Ketanserin is a new strong antiserotoninergic drug that, unlike the previous ones, is selective for 5-hydroxytryptamine receptors. This drug has been employed successfully in the treatment of arterial hypertension and of some peripheral vascular diseases. The authors are carrying out a trial on medium term treatment with ketanserin (K) or propranolol (P) in comparison with placebo, to evaluate their effects on blood pressure, haemocoagulative parameters and peripheral circulation. The trial is a double-blind cross-over random trial on subjects with mild or moderate hypertension. Until now 13 patients have ended the study; six of them are suffering from arteriosclerosis obliterans of the lower limbs at 1st or 2nd stage according to Fontaine. Both propranolol and ketanserin significantly reduced the blood pressure, although the decrease in systolic blood pressure was more evident after propranolol. Heart rate diminished significantly only after propranolol administration. The noninvasive, intermittent (every 30 min) monitoring of blood pressure showed a significant 24-hour reduction of blood pressure after administration of propranolol or ketanserin without significant changes of circadian behaviour of the blood pressure. After administration of ketanserin a slight improvement in peripheral circulation was demonstrated, evaluated by using strain-gauge plethysmography. As regards the results obtained for platelet function and other haemocoagulative parameters examined, adenosine diphosphate-induced platelet aggregation, adenosine diphosphate slope, collagen lag period, antithrombin III biological activity, and serum fibrinogen did not show noticeable modifications after treatment, while beta-thromboglobulin levels decreased slightly after ketanserin administration.

The reduction of total and LDL cholesterol (TC and LDLc), apoprotein B (ApoB) and in some instances triglycerides (TG) and the increase of HDL cholesterol (HDLc) and apoprotein A (ApoA) seem to be associated to a reduced coronary risk. Aim of our work was to evaluate the effects of a chronic treatment with the HMG-CoA reductase inhibitor simvastatin (MK-733), in a group of 8 dyslipidemic patients, 5 women and 3 men, aged between 48 and 69 years (mean age 59 +/- 8 years) at high risk being already affected by clinical compliances of atherosclerosis and not previously controlled by diet and/or other antidyslipidemic drugs. At the beginning and at the end (6 months) of this open study it was performed a clinical, ECG and ophthalmological examination, as well as an evaluation of the routine laboratory parameters. The initial dosage of simvastatin was a tablet of 10 mg/day, increased after a month to 20 mg and then to 40 mg/die. The mean dosage was 26.25 mg at the 3rd month and 21.25 mg at the 6th. Long-term simvastatin treatment was well tolerated (lack of important side effects as well as of significant changes of other clinical and laboratory parameters) and effective, reducing significantly (p less than 0.01) TC (317.9 +/- 30.8 vs 238.5 +/- 37.9 mg/dl), LDLc (210.6 +/- 48 vs 147.9 +/- 52 mg/dl), ApoB (144.7 +/- 17.5 vs 104.5 +/- 18), and TG (272.9 +/- 184 vs 200.5 +/- 117.6 mg/dl) and increasing in contrast HDL and ApoA values.(ABSTRACT TRUNCATED AT 250 WORDS)