[Therapeutic approach to arterial hypertension: comparison and combination of acebutolol with nifedipine and captopril].
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Publications and source records attributed to S Fazio.
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The antihypertensive efficacy and the acceptability of nifedipine (NI, Adalat) and the usefulness of its combination with a beta 1-selective blocking drug, acebutolol (AC), were studied in a placebo controlled trial on 15 patients with moderate hypertension. The study consisted of three phases: 1. An acute test, including the single blind comparison of three different single doses of NI (5, 10, 20 mg), alone and in combination with AC 200 mg, with placebo and with AC alone (200 mg), showed an early hypotensive effect, with no differences for the three doses of NI, reaching the maximum between 50 and 240 min, greater than the one of AC, and smaller in comparison with the one of the combinations, which didn't differ at the three doses of NI. Heart rate (HR) and side effects, instead, increased with the increasing doses of NI, suggesting a worse acceptability for the greater doses. 2. A long-term treatment, including a double-blind comparison of three separate periods of 4 weeks of treatment with NI (10 mg three times a day), AC (200 mg three times a day) and with the combination of the same doses, showed a significant reduction of systolic and diastolic blood pressure (BP) for each treatment, not significantly different at rest for the three single drugs but greater for the combined treatment, assuring also a better control of systolic BP during exercise. A reduced number of side effects was seen with the combined therapy which seems to contribute to a better compliance.(ABSTRACT TRUNCATED AT 250 WORDS)
Fifteen out-patients with moderate hypertension were randomly and sequentially treated with atenolol, indapamide and a combination of the two drugs after a wash-out period of at least 1 week and a 2-week placebo run-in period. The duration of treatment was 4 weeks in each case. The dosage was 2.5 mg indapamide and 100 mg atenolol, in single tablets which were taken at 11.00 hours. All the treatment regimens produced a highly significant (p less than 0.001) reduction in systolic and diastolic, supine and standing blood pressure; these reductions were not significantly different for the single drugs but were significantly greater for the combined therapy. The number of patients reaching the end-point of a diastolic blood pressure of 95 mmHg or less was the same with either atenolol or indapamide, i.e. 7 (46.6%), but was greater with the combined therapy, i.e. 10 (66.6%). A significant (p less than 0.001) reduction in pulse rate was observed with the treatments involving atenolol. Acceptability of the treatments was very good; the number of volunteered and elicited complaints during the different treatments being less compared to the placebo period, particularly for the combined treatment. No significant difference was observed in the blood biochemistry tests. The results are discussed in light of the mechanisms of action of the two drugs, which seem well integrated with each other, and the duration of the antihypertensive effect, which allows a single administration with consequent good treatment compliance.
We studied 10 obese volunteers, mean age 36.5 +/- 10.3 years, who weighed 123.56 +/- 28.7 g and were 69.96 +/- 22.5 kg overweight. The subjects did not have diabetes, arterial hypertension or signs of cardiac and respiratory failure or disease and all underwent right- and left-heart catheterization. cardiac output and stroke volume were high, according to increased oxygen consumption and to the degree of obesity. Ventricular end-diastolic and atrial pressures ranged from normal to high and correlated with body weight, signs of volume overloading and reduced left ventricular (LV) compliance. The mean pulmonary artery pressure was elevated and correlated well with weight, pulmonary resistance being normal; mean aortic pressure did not correlate with weight, and systemic arterial resistance tended to have a negative correlation. The LV function curve showed impaired ventricular function, particularly for the heaviest subjects, in whom Vmax and the ratio of the stroke work index to LV end-diastolic pressure were reduced. These indexes correlated well with each other and both correlated negatively with the degree of obesity. In contrast, maximal dP/dt was normal and did not correlate with excess weight. These observations show that depressed LV function is already present in relatively young obese people, even if they are free from signs of cardiopathy and other associate diseases. The degree of impairment of heart function seems to parallel the degree of obesity.
A case of hypereosinophilic syndrome showed clinical and hemodynamic signs of Löffler's endomyocardiopathy. The case is peculiar because of the young age, the early diagnosis, the lack of clinical and hemodynamic signs of heart failure. Some peculiarities: an apical diastolic murmur and a diastolic pulmonary capillaries/left ventricle pressure gradient recalled the picture of mitral stenosis, but the echocardiographic pattern of mitral valve was normal; a sistolic aortic and pulmonary subvalvular gradient, with an increase in ventricular wall thickness, was present. Echocardiography, systolic time intervals, and maxdp/dt and Vmax showed a very good left ventricular function. The patient is still in good compensation, with unchanged clinical pattern and eosinophilia, despite the therapeutical attempt with corticosteroids and antiallergic drugs, after one year from the diagnosis. The pathogenetic hypothesis of this cardiac and hematologic disorder are discussed.
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OBJECTIVE: The purpose of this study was to pilot test a self-administered chest pain questionnaire, a revised version of the Chest Discomfort Diary (CDD-R), in a sample of patients with chronic angina selected from a population known to have low literacy. DESIGN: The study design was descriptive and correlational. SAMPLE: The study used a convenience sample of 27 subjects with documented history of coronary artery disease and angina. Characteristics of the sample included a mean age of 56.3 years (SD, 12.4 years), 88.9% African-American, and 56.3% male, and 59.3% had a history of acute myocardial infarction. Approximately 28% had achieved a 9th-grade education or less, and reading levels ranged from 4th grade to 12th grade. Subjects completed the CDD-R, a 36-item instrument reflecting multiple dimensions of anginal chest pain. RESULTS: Descriptions of the location (left chest, 66.6%), character (pressure, 59.2%), and precipitants of chest pain (walking, 51.8%) were consistent with clinical descriptions of "typical angina." Other physical symptoms such as shortness of breath (88.8%) and fatigue (85.1%) were reported. Walking (55.5%) was the activity most frequently described as difficult to perform because of chest pain, with sublingual nitroglycerin (77.7%) the most frequently used and most effective chest pain relief strategy. CONCLUSION: The CDD-R adequately measured multiple characteristics of anginal chest pain. Further research is needed to establish construct validity of the CDD-R and to determine the feasibility of using the instrument to monitor changes over time in patients' chronic angina.
Until a few years ago, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) were considered essential only to the control of linear growth, glucose homeostasis, and for the maintenance of skeletal muscle mass. A large body of evidence recently coming from animal and human studies has unequivocally proven that the heart is a target organ for the GH/IGF-1 axis. Specifically GH exerts both direct and indirect cardiovascular actions. Among the direct effects, the ability of GH to trigger cardiac tissue growth plays a pivotal role. Another direct effect is to augment cardiac contractility, independent of myocardial growth. Direct effects of GH also include the improvement of myocardial energetics and mechanical efficiency. Indirect effects of GH on the heart include decreased peripheral vascular resistance (PVR), expansion of blood volume, increased glomerular filtration rate, enhanced respiratory activity, increased skeletal muscle performance, and psychological well-being. Among them, the most consistently found is the decrease of PVR. GH may also raise preload through its sodium-retaining action and its interference with the hormonal system that regulates water and electrolyte metabolism. Particularly important is the effect of GH on skeletal muscle mass and performance. Taking into account that heart failure is characterized by left ventricular dilation, reduced cardiac contractility, and increase of wall stress and peripheral vascular resistance, GH may be beneficial for treatment of heart failure. Animal studies and preliminary human trials have confirmed the validity of the GH approach to the treatment of heart failure. Larger placebo-controlled human studies represent the main focus of future investigations.
Three gross rearrangements of the low density lipoprotein receptor (LDL-R) gene were recognized during a survey of 23 unrelated Italian subjects with familial hypercholesterolemia (FH). Restriction endonuclease data were obtained by Southern blotting and hybridization with exon-specific probes. Proband FH-29 is heterozygous for a 4-kb deletion, which eliminates exons 13 and 14. This mutation is similar to that previously reported by other investigators in one Italian homozygous and two British and Canadian heterozygous patients. Proband FH-30 is homozygous for a 5.5-kb insertion caused by a duplication of exons 16 and 17 of the LDL-R gene. LDL-R mRNA isolated from skin fibroblasts of FH-30 was found to be larger than normal mRNA (5.6 versus 5.3 kb), in concordance with the insertion of the 236 nucleotides corresponding to exons 16 and 17. Proband FH-44 was found to have greater than 25-kb deletion, which eliminates the first six exons and the promoter region of the gene. This is the first example of a deletion that eliminates the promoter as well as the ligand-binding domain of the LDL-R gene. In the skin fibroblasts of this patient, the level of LDL-R mRNA was approximately half that found in control fibroblasts. We designate the new mutations found in FH-30 and FH-44 as FHviterbo and FHBologna-1, respectively, after the names of the Italian cities where the two patients were born.
A total of 10 patients with mixed angina were entered into a study to compare the anti-ischaemic efficacy of atenolol and amiodarone. The study was divided into three parts: (a) placebo for 2 weeks; (b) 100 mg atenolol given for 8 weeks; and (c) amiodarone given for 8 weeks, divided into week 1, 200 mg three times daily; week 2, 200 mg twice daily; weeks 3 and 4, 200 mg once daily; weeks 5-8, 200 mg once daily for 5 days a week. Clinical examination, basal and multi-stage effort electrocardiograms were performed at the end of each treatment. The number of anginal attacks and the amount of trinitrin taken by the patients were significantly reduced by both drugs with no significant difference between them. Compared with placebo, both drugs induced a significant increase in work capacity and in the time to decrease the ST-segment by 1 mm. At rest, atenolol reduced systolic blood pressure, heart rate and the systolic blood pressure--heart rate product compared with placebo. Systolic blood pressure was also reduced significantly compared with patients given amiodarone. Amiodarone did not influence these parameters. At maximum effort, amiodarone reduced heart rate and the systolic blood pressure--heart rate product compared with placebo. This reduction was greater for atenolol. The ST-segment depression was comparable between patients given either test drug. Amiodarone, therefore, exerts an anti-ischaemic effect similar to that shown by atenolol with different haemodynamics: atenolol reducing myocardial oxygen demand, amiodarone having an additive increase of coronary flow. Such an effect was obtained with a lower dose of amiodarone than is commonly used.
Carotid atherosclerotic lesions can be studied with color-Doppler ultrasonography vascular systems. Ultrasonography of the carotid plaques at major risk for the development of cerebrovascular ischemic events showed the following characteristics: irregular surface, degree of stenosis > 70%, intimal hemorrhage and ulceration. The plaques with these ultrasonography patterns have to be considered for surgical approach (TEA). The other patients with carotid atherosclerotic lesions will be initially treated with diet and changes of life style to obtain the correction of cardiovascular risk factors (i.e. hypertension, hypercholesterolemia, diabetes). Furthermore, medical therapy with antithrombotic agents will be instituted which, used with good results also in acute cerebral stroke, proved to be effective in the reduction of vascular events in patients with extracranial atherosclerotic plaques. However, it has not been clarified if the positive effect of antiaggregation therapy in carotid atherosclerosis is due to the inhibition of the progression and plaque growth or if other hemorheological factors are involved.
A group of normotensive obese subjects (group A), a group of hypertensive obese subjects (group B) and a group of control subjects (group C) were submitted to radionuclide ventriculography using 99mTc to investigate cardiac function and haemodynamic situation in the presence of an increased preload (group A), preload and afterload (group B). Results show a significant reduction in ejection fraction and systolic blood pressure/end systolic volume in group A. Group B shows better cardiac function probably for the presence of cardiac concentric hypertrophy. Left ventricle work either in a minute and for each beat is greatest in patients of group B. Thus the simultaneous presence of obesity and hypertension can cause a worse prognosis in such patients for cardiac ischaemia and/or sudden death.
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