Photo quiz. Oriental sore (old world cutaneous leishmaniasis).
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Biomedical subjects
Publications and source records attributed to G Ghigliotti.
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The aim of this study was to evaluate the efficacy and possibly the mechanism of action of gallopamil and diltiazem in a double-blind crossover trial in patients with effort ischaemia. Twenty male patients (mean age 57 +/- 6 years) with documented coronary atherosclerosis and exercise-induced ischaemia (ST depression greater than or equal to 0.15 mV) completed the study, which consisted of four 7 day periods. At the end of each period a multistage bicycle exercise stress test was performed under placebo (first and third periods) and randomly under gallopamil (50 mg t.i.d.) or diltiazem (90 mg t.i.d.) in the second and fourth periods. Both drugs significantly increased time to ischaemia (0.15 mV ST depression) as compared to placebo, from 7.9 +/- 1.7 min to 8.9 +/- 1.1 min (diltiazem) and 9.1 +/- 1.6 min (gallopamil) with no significant difference between the two drugs, and reduced the maximal extent of ST shift from 0.18 +/- 0.08 mV to 0.13 +/- 0.04 mV (diltiazem) and 0.12 +/- 0.05 mV (gallopamil). Analysis of the results from the whole population showed that the beneficial effect did not appear to be related to any specific parameter. Individual analysis showed that 13/20 patients under gallopamil and 13/20 under diltiazem increased time to ischaemia, while this was unchanged or reduced in the remainder. A positive correlation between changes in time to ischaemia and changes in rate x pressure product at ischaemia was found in both those administered gallopamil (R 0.80, P less than 0.01) and diltiazem (R 0.65, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
A 43-year-old homosexual man with the Acquired Immunodeficiency Syndrome (AIDS) developed cutaneous molluscum contagiosum-like lesions on face, ears, neck, hands and feet. He was admitted to our unit with fever, malaise and headache. Cytologic examination of skin brushing revealed numerous encapsulated budding yeasts, identified as Cryptococcus neoformans. Such a finding calls for a cytologic examination of skin lesions in patient with AIDS who present with fever and headache, in order to rule out a potentially life-threatening fungal infection.
A 24-year old male patient developed, on both legs, lesions typical of Mibelli's porokeratosis 22 months after bone marrow transplantation, under treatment with cyclosporin A. He denied any family history. Mibelli's porokeratosis seldom develops after an immunosuppressive treatment, and to our knowledge it has exceptionally been described after bone marrow transplantation. A possible complication of Mibelli's porokeratosis is the development of Bowen's disease, basal or squamous cell carcinomas. Immunosuppressive treatment might facilitate the degeneration. For this reason, these subjects should be periodically and carefully examined.
Multiple drug therapy, including nitrates, beta blockers, calcium antagonists, aspirin, and heparin, has been advocated as effective in the treatment of unstable angina, a syndrome with a multifactorial pathogenesis. Recently, plaque rupture and thrombosis have been demonstrated as the most important pathogenetic mechanisms. Nevertheless, clear-cut results on the effects of thrombolytic treatment in unstable angina are still lacking. Some possible explanations why the medical treatment of unstable angina has still not yet been standardized, whereas that of myocardial infarction has, are suggested. A review of randomized and nonrandomized studies published on this topic evaluating the role of different thrombolytic agents in unstable angina is presented. In addition the role of coronary angiography is discussed. In view of the disappointing results of coronary artery bypass surgery performed in the acute phase of the disease, one of the goals of clinical research is to identify subsets of patients at high and low risk and who undergo different types of therapeutic interventions. To support published data suggesting that total myocardial ischemia has a significant impact on prognosis, we present our results of a study carried out on patients with refractory unstable angina treated with thrombolytic therapy and evaluated with continuous electrocardiographic monitoring in the attempt to correlate total myocardial ischemia with short-term prognosis. Data in favor of the prognostic role of continuous electrocardiographic monitoring in unstable angina are also reviewed. Finally, we propose some suggestions that might be useful for future studies.
We tested the safety and the usefulness of intravenous urokinase (2 million units administered over 30 min) in 44 patients with refractory unstable angina, defined as persistence of ischemic episodes during 48-h Holter monitoring (Phase 1) despite maximal medical therapy. After thrombolysis, recurrence of ischemia was observed during a week of observation in the CCU, including two 24-h Holter monitorings at the beginning and the end of the week (Phase 2). Seventeen patients completed the observation period without either symptomatic or asymptomatic ischemic episodes (Group A); the remaining 27 continued to manifest ischemia (Group B). No bleeding complications occurred. Within a 6-month follow-up, 2 patients of Group A had recurrence of unstable angina while in Group B, 19 patients had refractory angina or a major cardiac event [10 patients underwent coronary artery bypass surgery (CABG) or percutaneous transluminal coronary angioplasty (PTCA) for refractory angina (p less than 0.001), 6 other patients with refractory angina continued medical therapy, one patient had a myocardial infarction, and two patients died]. In Phase 1 the duration of total ischemia (min/24 h) was a relevant prognostic marker: higher duration correlated with adverse clinical outcome (p less than 0.01). In comparison to Phase 1, duration of total ischemia in Phase 2 was significantly reduced in both groups (16.9 +/- 19.6 vs. 25.4 +/- 17.7; p less than .001). A percent value expressing this variation was calculated for each patient: the variation thus obtained again gave information on the clinical outcome--the greater the reduction, the lower the risk of cardiac events (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
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Congestive heart failure is a syndrome with multiple causes and manifestations. While rheumatic heart disease and hypertension are in decline, coronary artery disease is the leading cause in patients referred for evaluation of heart failure. Decrease in cardiac contractility and general neurohormonal activation, which trigger alterations in mechanical and biochemical factors in cardiac muscle and bring derangements of haemodynamics, are now considered as excessively early compensatory mechanisms which can be regarded as deleterious in patients with heart failure. Therapeutic principles illustrated in this article emphasize the importance of basic research and clinical observations derived from trials set the stage for therapeutic interventions. The approach to the patient with silent myocardial dysfunction must be treated so as to have the greatest beneficial impact on the prognosis of this disease.
The decision to treat hypercholesterolemia must take into account both the risk of death and myocardial infarction and the risk/benefit ratio of treatment. Nowadays there is convincing evidence that hypercholesterolemia in patients with previous myocardial infarction is an important prognostic factor: furthermore, the excess of risk due to cholesterol is consistently higher than that in the general population. Prospective studies demonstrated that cholesterol lowering treatment obtained either with diet or drugs can improve survival and quality of life in postinfarction patients. Experimental, clinical and angiographic studies suggested that cholesterol lowering therapy can produce both stabilization and regression of the atherosclerotic plaque. In view of this, the evaluation of cholesterol level must be part of the general work-up of patients with previous myocardial infarction. The satisfactory results obtained with diet suggest to try a dietary treatment in post-infarction patients with high cholesterol level before using drugs. Since there are no clear-cut upper values, the end point of treatment should be to lower cholesterol levels to the values recommended for the general population, although we believe that threshold values to be obtained in these subjects should be lower than those requested in primary prevention.
The aim of the study is to evaluate the reproducibility of exercise testing and to determine whether there is any correlation between the reproducibility of exercise test and response to the ergonovine maleate test. Thirty-eight patients with mixed angina and documented coronary artery disease underwent an ergonovine maleate test and four exercise tests on consecutive days in the same basal conditions. The ergonovine test was positive in 20 patients (Group I) and negative in 18 patients (Group II). There were no significant differences in the clinical and angiographic data of the two groups. All 152 exercise tests were positive. The variability of the response of the repeated tests was assessed by means of an analysis of the following parameters: heart rate, blood pressure, rate-pressure product, watts, and minutes were recorded at the onset of ischemia (ST decreases greater than or equal to 0.1 mV). Range (maximal-minimal obtained value), ratio between range and maximal obtained value, and coefficient of variation (standard deviation/mean of the four parameters) were calculated for each patient. The analysis of these values demonstrated that while the test was reproducible in some patients, a high individual variability was present in others. Moreover, the individual variability results were higher in Group I than in Group II, with a statistically significant difference for all considered parameters. In conclusion, it is possible to have a poorly reproducible exercise test in patients with mixed angina. The correlation between a positive ergonovine test and a poorly reproducible exercise test suggests that abnormal coronary vasomotion may sometimes be present during exercise and may affect the reproducibility of the test.
Twelve of 40 consecutive patients with effort angina, documented coronary artery disease, and a positive exercise stress test had a positive ergonovine test. ST-segment depression (0.1 mV) occurred in ten and ST elevation (0.1 mV) in two patients. During the ergonovine maleate test the rate-pressure product recorded at the onset of ischemia (ST greater than or equal to 0.1 mV) was significantly lower than that recorded during the exercise stress test. The reproducibility of the rate-pressure product at ischemia was displayed in every patient with a second test; then, a third test after intravenous nifedipine infusion (1 mg over 5 minutes + 1 mg over 55 minutes) was performed. Six patients had negative results; out of the remaining six, three exhibited a significant increase in the dosage required for provoking ischemia. Both systolic and diastolic blood pressure were reduced by nifedipine, while only a slight increase in heart rate occurred, so that the rate-pressure product at any ergonovine dosage was decreased by nifedipine. No differences in the ischemic threshold during exercise and during the ergonovine maleate tests (in washout and after nifedipine) were found in patients with a positive or negative response to nifedipine. The ergonovine test was positive in a sizable (30%) number of patients with stable effort angina. In these patients nifedipine was effective in preventing ergonovine-induced myocardial ischemia.
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We tested the safety and the usefulness of intravenous fibrinolysis in 44 patients with refractory unstable angina, defined as persistence of ischemic episodes during 48-hour Holter monitoring (phase 1) despite maximal medical therapy. After fibrinolysis, recurrence of ischemia was recorded during 1 week of observation in CCU including 2 24-hour Holter monitoring at the beginning and at the end of this week (phase 2): 17 patients completed the observation period without either symptomatic or asymptomatic ischemic episodes (Group A); the remaining 27 patients continued to manifest ischemia (Group B). No bleeding complications occurred. Within a 6-month follow-up, 2 patients of Group A had recurrence of unstable angina while in Group B, 10 patients underwent CABG or PTCA for refractory angina, 6 other patients with refractory angina continued medical therapy, 1 patient had a myocardial infarction and 2 patients died (p less than 0.001). Phase 1: the duration of total ischemia (min/24 hours) was a relevant prognostic marker: higher duration correlated with adverse clinical outcome (p less than 0.01). Phase 2: in comparison with phase 1, duration of total ischemia was significantly reduced (p less than 0.001). A percent value expressing this variation was calculated for each patient: (min of ischemia in phase 2 - min of ischemia in phase 1/min of ischemia in phase 1). The variation thus obtained again gave information on the clinical outcome: the greater was the reduction, the lower was the risk of cardiac events (p less than 0.001). Our data suggest that: clinical stabilization may be obtained with the addition of fibrinolysis to conventional treatment; Holter monitoring bears prognostic information helpful in identifying patients who need further intervention.
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