Influence of climatic variables on acute myocardial infarction hospital admissions.

BACKGROUND: Seasonal peaks in acute myocardial infarction (AMI) incidence have been widely reported. Weather has been postulated to be one of the elements at the basis of this association. The aim of our study was to determine the influence of seasonal variations and weather on AMI hospital admissions. METHODS: We correlated the daily number of AMI cases admitted to a western Sicily hospital over twelve years and weather conditions on a day-to-day basis. Information on temperature, humidity, wind force and direction, precipitation, sunny hours and atmospheric pressure was obtained from the local Birgi Air Force base. A total of 3918 consecutive patients were admitted with AMI over the period 1987-1998 (2822 men, 1096 women; M/F: 2,58). RESULTS AND CONCLUSIONS: A seasonal variation was found with a significant winter peak. The results of multivariate Poisson analysis show in both sexes a significant association as regards the incidence relative ratio between the daily number of AMI hospital admission and minimal daily temperature and maximal daily humidity. The incidence relative ratios (95% confidence intervals) were, in males, 0.95 (0.92-0.98) (p<0.001) as regards minimal temperature and 0.97 (0.94-0.99) (p=0.017) as regards maximal humidity. The corresponding values in females were respectively 0.91 (0.86-0.95) (p<0.001) and 0.94 (0.90-0.98) (p=0.009). Environmental temperature, and also humidity, may play an important role in the pathogenesis of AMI. These data may help in understanding the mechanisms whereby AMI events are triggered and in organizing better the assistance to ischemic patients throughout the year.

Effects of drug therapy on cardiac arrhythmias and ischemia in hypertensives with LVH.

Left ventricular hypertrophy (LVH) in hypertensive subjects is associated with an increased prevalence of ventricular arrhythmias. To evaluate the effect of antihypertensive treatment on cardiac arrhythmias (CA) and transient episodes of myocardial ischemia (TEMI), we studied 46 hypertensive patients with LVH, divided into four groups randomly treated with enalapril, hydrochlorothiazide (HCTZ), atenolol, or verapamil (SR-V) for 6 months. Office blood pressure and office heart rate values were recorded, in basal conditions, after 1 and 6 months of treatment, and all patients underwent echocardiography, electrocardiographic Holter monitoring, and stress testing. All drugs significantly lowered blood pressure, whereas left ventricular mass index was reduced by atenolol, enalapril, and SR-V, but not by HCTZ. Treatment induced a significant reduction in the number of patients with supraventricular arrhythmias (35 v 15, P < .034, and 28 v 8, excluding patients treated with HCTZ, P < .008). The number of patients with ventricular arrhythmias was also reduced (32 v 16 considering all groups, P < .08, and 24 v 9, excluding patients treated with HCTZ, P < .04). The number of TEMI during Holter monitoring significantly decreased from 47 to 23 (P = .043) in all patients, and from 39 to 14 (P = .013) excluding patients treated with HCTZ. In all groups, irrespective of treatment, a reduction of blood pressure, heart rate, and systolic blood pressure/heart rate product measured by exercise stress test was observed. The present study shows that in hypertensive patients with LVH, antihypertensive treatment with atenolol, enalapril and SR-V reduces LVH and decreases the prevalence of CA and TEMI. Treatment with HCTZ during the 6-month study did not alter LVH and did not appear to reduce CA and TEMI.

Increased plasma levels of fibrinogen in acute and chronic ischemic coronary syndromes.

BACKGROUND: 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. METHODS: 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. RESULTS: Plasma levels of fibrinogen were higher in patients with chronic ischemic heart disease (335.3 +/- 81.2 mg/dl, p < 0.001) and especially in patients with acute myocardial infarction (454.72 +/- 69.5 mg/dl, p < 0.00001) and unstable angina (382.6 +/- 101.3 mg/dl, p < 0.00025) 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, p < 0.02). 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, p < 0.00001) 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. CONCLUSIONS: 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.

Increased prevalence of cardiac arrhythmias and transient episodes of myocardial ischemia in hypertensives with left ventricular hypertrophy but without clinical history of coronary heart disease.

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.

Behaviour of arm venous pressure in patients with systodiastolic hypertension and in the elderly with isolated systolic hypertension in comparison with healthy controls.

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) (p<0.001). 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, p<0.0001). Considering ten subjects, matched for sex and age in each group, we observed again that VP values in SDH were >ISH>CS (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, p<0.001). In all three considered groups a significant correlation between the values of SBP and DBP with VP (p<0.001) 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.

Effects of captopril and ticlopidine, alone or in combination, in hypertensive patients with intermittent claudication.

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: prevalence, prognostic significance, diagnosis]. / Ischemia miocardica silente: prevalenza, significato prognostico, diagnostica.

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.

[The physiopathology of critical ischemia of the lower limbs]. / Fisiopatologia dell'ischemia critica degli arti inferiori.

Peripheral obstructive arterial disease (POAD) of the lower limbs is the third main complication of atherosclerosis, after coronary artery disease and cerebrovascular disease. In 15-20% of cases POAD have an unfavourable evolution toward critical leg ischemia (CLI). This clinical condition is characterized by the onset of rest pain and/or trophic cutaneous lesions until gangrene appears. In some cases amputation is needed. The pathophysiological, clinical and therapeutic aspects of CLI were recently discussed in two Consensus Conferences held in Berlin in 1989 and in Rudesheim in 1991, with the elaboration of a final draft published on circulation. CLI appears when peripheral perfusion critically decreases due to macro and microcirculatory alterations. Atherosclerotic plaque is the primum movens, but often there are more plaques in sequence along the ilio-femoro-popliteal axis. The pathophysiological and clinical consequences are more severe if the stenosis is haemodynamically important, after a rapid progression of plaque growth or when thrombotic complications develop. The reduction in distal perfusion induces troubles in the microcirculation and an embalancement between the microvascular defense system (MDS) and the microvascular flow regulating system (MFRS) with endothelial dysfunction, platelet and leucocytes activation, worsening of blood viscosity due to the increase in fibrinogen levels and to the red cells deformability changes, activation of coagulation and impairment of fibrinolysis. So, a vicious circle appears with further worsening of distal perfusion and onset of trophic lesions. A further worsening of CLI can derive from local recurrent infections particularly frequent in diabetic patients.

Hypertension and other risk factors in peripheral arterial disease.

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 (p < 0.01) 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.

Regression of structural vascular changes in hypertensives after captopril treatment.

In order to investigate whether hypertension-related structural vascular changes may be influenced by antihypertensive treatment, 10 patients were studied suffering from essential arterial hypertension, five males and five females, aged between 34 and 61 years (mean age: 46.9 +/- 8.13 years). All patients received a placebo for 1 week and then captopril, 75 mg b.i.d. for 3 months. After placebo and captopril treatments, the following parameters were evaluated: SBP, DBP, mean blood pressure (MBP), by the formula 1/3 (SBP + 2 x DBP) and basal and minimal vascular resistances, respectively obtained by the ratios MBP/rest flow and MBP/peak flow. Blood flows have been obtained by strain gauge plethysmography. A significant decrease in systolic (P less than 0.025), diastolic (P less than 0.01) and mean blood pressure (P less than 0.01), basal vascular resistances (52 +/- 19 vs 28 +/- 12 A.U., P less than 0.01) and minimal vascular resistances (6.3 +/- 2.2 vs 3.9 +/- 2.8 A.U., P less than 0.025) has been observed after captopril treatment in comparison to placebo, whereas rest (2.9 +/- 0.7 vs 4.1 +/- 0.9 ml.min-1.100 g-1, P less than 0.01) and peak blood flows (21.3 +/- 5.8 vs 29.7 +/- 9.4 ml.min-1.100 g-1) significantly increased. These data seem to indicate that antihypertensive treatment with the angiotensin-converting enzyme inhibitor, captopril, is not only efficacious in inducing a significant blood pressure decrease, consequent to the reduction of basal vascular resistance (due to the vasodilating effects of the drug), but is also able to reduce minimal vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence of risk factors in patients with peripheral arterial disease. A clinical and epidemiological evaluation.

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 (p < 0.01) 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.

Partial regression of vascular structural alterations in hypertensive patients treated with alpha-beta-blocker, labetalol.

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.

Cardiovascular structural changes in hypertension: possible regression during long-term antihypertensive treatment.

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.

[Vascular damage in arterial hypertension: its noninvasive assessment]. / Il danno vascolare nell'ipertensione arteriosa: valutazione non invasiva.

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.

[Acute effects of transdermal administration of nitroglycerin on effort tolerance and myocardial perfusion, evaluated by Tl-201 scintigraphy, in patients with stable effort angina]. / Effetti acuti dell'applicazione di nitroglicerina per via transdermica sulla tolleranza allo sforzo e sulla perfusione miocardica, valutata mediante scintigrafia con tallio 201, in pazienti con angina stabile da sforzo.

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.

[Cardiac arrhythmias in hypertensive subjects with and without left ventricular hypertrophy compared to the circadian profile of the blood pressure]. / Aritmie cardiache in soggetti ipertesi con e senza ipertrofia ventricolare sinistra in rapporto al profilo circadiano della pressione arteriosa.

To evaluate possible correlations between cardiac arrhythmias and circadian pattern of blood pressure (BP) and of heart rate (HR), we studied 2 groups of 20 males with stable arterial hypertension of mild to moderate entity, with (Group I) or without (Group II) left ventricular hypertrophy (LVH). In patients with LVH the mean age (56 vs 46 years), the duration of the hypertensive state (48.1 vs 15.7 months), the thickening of interventricular septum (IVS; 13.7 vs 9.6 mm) and of the posterior wall of the left ventricle (13.2 vs 9.2 mm) and the mass of LV (149.8 vs 99.7 g/m2) were significantly greater (p less than 0.01). On the contrary, the 2 groups did not show significant differences concerning casual BP determined in the morning (178.3/108.4 vs 171.5/106.2 mmHg). After a pharmacological washout of 2 weeks, patients underwent a noninvasive, intermittent, monitoring of BP (every 15 min during daytime and every 30 min from 11 pm to 7 am), using a pressure meter II Del Mar Avionics, and a continuous monitoring of ECG for 24 hours, employing an instrument 445/B Del Mar Avionics. Mean 24-hour BP was not different in the 2 groups of patients (161.7/99.0 vs 158.2/98.3 mmHg); however, patients with LVH showed a significantly greater variability of BP in the morning (7 am-3 pm), while mean 24-hour HR was significantly less (71.6 vs 78.2 b/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac arrhythmias as correlated with the circadian rhythm of arterial pressure in hypertensive subjects with and without left ventricular hypertrophy.

To evaluate the relationship among supraventricular and ventricular arrhythmias with blood pressure and heart rate (HR) values, we studied 2 groups of 20 hypertensive men with (group I) and without (group II) left ventricular hypertrophy. Ambulatory electrocardiographic tracings were recorded continuously, together with ambulatory arterial pressure. Systolic (SBP) and diastolic (DBP) blood pressure values measured over 24 h showed no difference between the two groups, but we found greater variability in SBP in group I. The incidence of ventricular and supraventricular arrhythmias was significantly higher in patients of group I; moreover, we found a strong correlation between the incidence of ventricular extrasystoles (VPCs) and SBP, DBP, and HR values in group I, whereas in group II the incidence of supraventricular extrasystoles (APCs) was higher during peaks of SBP and HR values. The relationship between APCs and SBP observed in group II may be attributable to the pressure stimulus on a normal atrium, and the significant correlation between VPCs and SBP, DBP, and HR values may be due to episodes of subendocardial ischemia or to the influence of adrenergic stimulation on previously compromised myocardial tissue.

[Effect of a long-term treatment with simvastatin, an inhibitor of HMG-CoA reductase, in dyslipidemic patients at high risk]. / Effetti di un trattamento cronico con simvastatina, un inibitore dell'HMG-CoA reduttasi, in pazienti dislipidemici ad alto rischio.

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)