Biomedical subjects
Publications and source records attributed to R Fogari.
Hypothermia is reflected in the electrocardiogram in the form of alterations that permit early recognition of the condition. In fact the electrocardiogram is a more sensitive indicator of temperature than the standard measurements of body temperature used in clinical practice. The various aetiological aspects of hypothermia are described as are its electrocardiographic features.
The aim of this study is to evaluate the effects of chronic beta-blocking therapy (atenolol 100 mg/d) on ECG and ECG indexes of left ventricular hypertrophy (LVH) in hypertensive patients. Seventy one subjects with essential hypertension (mean age 47 y) were studied for 5 years. Sokolow-Lyon voltage criteria for ECGLVH (S wave in V1 plus R wave in V5 greater than or equal to 35 mm) were employed in: 38 treated patients with ECGLVH, 12 treated patients without ECGLVH and 21 untreated patients with ECGLVH. Beta-blocking therapy significantly reduced blood pressure (BP) in the treated patients. In the patients with ECGLVH, treatment significantly improved Sokolow-Lyon Index (SLI) reducing it from 55.04 +/- 16.2 mm to 47.6 +/- 15.04 mm (p less than 0.05) but only 11.4% of the treated patients returned within the normality range (SLI less than 35 mm). No significant change was present in the treated patients without ECGLVH. On the contrary, the group of untreated patients showed an increase in SLI from 45.19 +/- 7.08 mm to 50.52 +/- 11.09 mm (p less than 0.05) and no change in hypertension levels. We conclude, therefore, that: ineffective BP control allows progression of LVH; BP reduction by beta-blocking drugs reduces LVH but does not produce complete regression of the hypertrophy, if not in the early stages; if no LVH is present, BP control by these drugs prevents LVH. We emphasize the importance of early detection and treatment of hypertension.
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The antihypertensive efficacy and tolerability of bisoprolol and atenolol were compared in the Bisoprolol International Multicenter Study (BIMS). In 104 patients with essential hypertension (21 to 70 years of age and diastolic blood pressures (DBP) of 100-120 mm Hg in the sitting position), after a four-week placebo period, the active drug was given in a random double-blind crossover design (10 to 20 mg bisoprolol, 50 to 100 mg atenolol) for eight weeks each, with a 2 to 6 week placebo wash-out phase between active therapy. All blood pressures were recorded 24 h after drug intake. Of the 104 patients, 10 were withdrawn during the study because of unwanted effects, unsatisfactory blood pressure response, or intercurrent disease, leaving 94 for intraindividual comparisons. After 8 weeks active treatment with individually titrated dose, there were slightly, but significantly greater falls in blood pressure with bisoprolol (p less than or equal to 0.05). Diastolic target pressures of less than or equal to 95 mm Hg were reached in 68% with bisoprolol and 56% with atenolol (p less than or equal to 0.05; Mc Nemar). There was no between treatment group difference in the patients' self-assessed well-being. For both drugs, response rates were greater in patients below the age of 60 years than in those above 60 years. Better antihypertensive responses were observed with bisoprolol in patients regularly smoking cigarettes.
Forty-five hypertensive patients (I-II WHO), after two weeks wash out, were randomly allocated to receive 100 mg/day atenolol, 200 mg/day metoprolol and 10 mg/day mepindolol for three months, in order to evaluate their possible effect on lipid metabolism. Plasma triglyceride levels were increased by the three drug treatments; the increase was, however, greater after mepindolol. Total cholesterol was unchanged by atenolol, increased by metoprolol and decreased by mepindolol. HDL-cholesterol was unchanged by atenolol, decreased by metoprolol and increased by mepindolol, whereas LDL-cholesterol was increased by atenolol, unchanged by metoprolol and decreased by mepindolol. Therefore, the LDL/HDL ratio was decreased by mepindolol (from 3.15 +/- 1.71 to 2.92 +/- 1.17) and increased by atenolol and metoprolol. The results show that the treatment with atenolol, metoprolol and mepindolol does not significantly affect the lipid levels suggesting that cardioselective beta-blockers as well as those with ISA have no untoward effect on lipid metabolism.
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To assess the influence of chronic atenolol therapy on the cardiovascular responses to isometric exercise, we evaluated the behavior of blood pressure, heart rate and double product in 75 hypertensive patients treated with atenolol 100 mg once daily for 6 months. During the 1st month of treatment, both systolic blood pressure (SBP) and diastolic blood pressure (DBP) increases rose more than before treatment. SBP increase to handgrip became lower than before treatment on the 2nd months of therapy (p less than 0.05) and fell even more afterwards (p less than 0.01 on the 6th month). On the contrary, DBP increase subsequently steadied on levels not significantly different from those before treatment. Double product increase was inferior to that recorded before atenolol administration; the difference became significant after 2 months and reached its apex after 6 months of treatment. The conclusion was that chronic atenolol therapy affected some cardiovascular responses to handgrip although to a different extent depending on treatment length; it would seem sensible to pay attention to how long a patient has been on beta-blocker when evaluating the response to isometric exercise.
The antihypertensive efficacy and tolerance of a new fixed combination of 50 mg atenolol and 12.5 mg chlorthalidone (Tenoretic Mite, TM) was studied in 37 patients with arterial hypertension, aged 61-80 years (mean, 70.2 years), who had been randomized to either 50 mg atenolol or 12.5 mg chlorthalidone for a 4-week period. At the end of this period, the fixed combination of atenolol and chlorthalidone was given to all patients for 6 months at a dose of one tablet daily in the morning. In both atenolol- and chlorthalidone-pretreated patients, treatment with the fixed combination resulted in a further significant drop in blood pressure, whereas the heart rate decreased only in the latter group. The mean blood pressure reduction achieved by the fixed combination was 30/15 mmHg in the standing position. Serum potassium levels significantly increased with the fixed combination compared with values on chlorthalidone alone. Unwanted effects were rare, and their frequency tended to decrease over time. In conclusion, the fixed combination of 50 mg atenolol plus 12.5 mg chlorthalidone tested in this study proved highly effective in lowering elevated blood pressure values in a population of elderly hypertensive patients treated over a 6-month period without noticeable unwanted effects.
A long-surviving clinical case of suspected Morquio's syndrome is described. The locomotorium (vertebral dwarfism, hyphoscoliosis, but no hypoplasia of the odontoid process of the epistropheus, platyspondylia), cardiopulmonary (aortic insufficiency, arterial calcification, varices) visual (opaque lens on right eye, sclerosis of the lenticular lamellae but no corneal opacity on left eye) acoustic (deafness) and gastroenteric systems (hepatomegaly) are analysed. No pathological granulations were noted in the leukocytes. The plasmatic lysosome enzymes were normal and alpha-fucosidase subnormal. Abnormal keratan sulphate secretion was noted in the daily urine. All this would explain the patient's long survival.
Response to sustained (three-minute) handgrip at one-third maximum contraction was studied in 75 subjects with essential hypertension. The patients responded with an increase in heart rate, systolic and diastolic blood pressure, and double product. Chronic atenolol therapy (100 mg/day in a single administration) decreased the values of these measurements at rest and during exercise. The treatment did not prevent or attenuate the rise in heart rate with grip, but it partially inhibited the pressor response to handgrip. Chronic atenolol therapy may reduce the risk of vascular disease by decreasing blood pressure and its response to isometric exercise. Additionally, chronic beta-adrenergic blockade with decreased heart rate, double product, and, most likely, myocardial oxygen consumption is probably a further cardioprotective factor.
We have studied the electrical behaviour of the skin on 20 volunteers, before and after cleaning with solid detergent. The aim was to study one of the possible variables of the measurements. The results have shown that the cleaning has globally reduced the electrical skin parameters of the forehead, without influencing other parts examined (dorsal and palmar surfaces of the hand). The result has been attributed to the elimination of the hydrolipidic film of the surface and in particular that of the sebum of the forehead. The data give an idea as to how to obtain more homogeneous final results, as well as studying the sebum production function.
In the normal young adults were studied electrical characteristics of the skin in five different regions. The results obtained have demonstrated presence of the topographic differences of the external resistance as well as capacity. It does not seem like that these differences can be correlated with the thickness at the corneal layer, but rather with the different glandular composition from one region to another and probably with the different hydration state of the skin. There were also demonstrated differences between sexes, characterized by the lower external resistance in males than in females.
To assess the influence of selective and nonselective beta blockers with or without ISA we evaluated the extent of pressor responses to isometric exercise in 15 hypertensive patients who had first been treated with atenolol (100 mg/day) and subsequently with mepindolol (15 mg/day) for 2 months each following placebo administration for 2 weeks. Isometric handgrip was always performed in a supine position. Blood pressure and heart rate were measured at 30% of the maximal voluntary contraction. The percentages of blood pressure increases associated with the isometric test were similar during treatment with the two beta blockers; only heart rate was significantly lower. Systolic and diastolic blood pressures showed a lower increase with mepindolol than with atenolol, but the differences were not statistically significant. In conclusion, cardioselective beta blockers without ISA and nonselective beta blockers with ISA influence systolic and diastolic blood pressure responses to a handgrip of 30% in the same way. Only heart rate shows a lower but rather small increase during the cardioselective drug treatment.
In view of the postulated association between plasma lipids and the development of atherosclerosis, there is growing interest in the effects of beta blockers on plasma lipids. This study was undertaken to investigate whether a nonselective beta blocker, such as mepindolol, which possesses intrinsic sympathomimetic activity, causes significant changes in serum lipids, particularly in their ditribution among the different lipoproteins. Eighteen healthy subjects, twelve males and six females, were given mepindolol orally, daily doses of 0.2 mg/kg averaging 10-15 mg. Pre- and post-treatment fasting total serum cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides were evaulated; the ratio LDL cholesterol/HDL cholesterol was also calculated. Total cholesterol did not change significantly after treatment with mepindolol (- 1.9 mg%), whereas a small and nonsignificant decrease was observed in LDL cholesterol (- 6 mg%); no change was found in HDL cholesterol (- 0. mg%). Serum triglycerides showed a significant increase (+ 20.9 mg%, p less than 0.01). Thus, the most prominent effect of even a short period of treatment with mepindolol is a net increase in serum triglyceride levels. It must be remembered that high triglyceride levels do not constitute a cardiovascular risk factor. On the other hand, no significant changes in total cholesterol, HDL and LDL cholesterol, and in LDL cholesterol/HDL cholesterol ratio were observed. The results of this study show that mepindolol, unlike other beta-blocking agents, does not affect cholesterol concentration and distribution among the lipoproteins. In particular it does not reduce HDL cholesterol, which is currently assumed to be inversely related to the development of atherosclerosis.
Although policardiography has been in use for more than a century, only recently attention has been focused on instrumental and methodological problems of the technique. Among these, frequency response and time constant of the equipment are in first place. Time constant must be long enough to allow an accurate recording of the low and ultra-low frequency vibrations which are generated in the cardio-aorto-hemic system, in particular of those constituting the carotid pulse and the apexcardiogram. The authors stress the influence that incidental air leaks in the recording assembly, or type and size of the pickup device, have on the value of the time constant. Kinetocardiography seems preferable to apexcardiography in order to reproduce with higher fidelity absolute movements of the anterior thoracic wall in every single point.
Systolic intervals, heart rate (HR) and blood pressure (BP) were monitored before and after oral administration of dilazep in 28 patients with chronic coronary disease. Controls were performed before drug assumption and after two months of treatment. 16 patients were given dilazep in 100 mg doses three times a day; 12 patients in 50 mg doses three times a day. In the former group dilazep brought about a PEP reduction owing to a shortening of the isovolumic contraction time. Also we noticed a constant decrease of BP, both systolic and diastolic, the former tapering from 155 down to 143 mmHg, the latter from 88 to 81. In the 12 patients treated with 150 mg a day, we did not notice any relevant alteration relatable to the drug since systolic intervals and BP were unimpaired. These observations point to a positive inotropic effect and a moderate vasodilatatory effect caused by dilazep if administered in 300 mg doses a day.
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