Vasotonic angina: a spectrum of ischemic syndromes involving functional abnormalities of the epicardial and microvascular coronary circulation.

OBJECTIVES: The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia. BACKGROUND: Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous anginal attacks or exercise stress testing. METHODS: Twenty-five patients with no or minimal (< 30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina). RESULTS: Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 +/- 4%) and those with coronary artery disease (5 +/- 3%) but severe (p < 0.001) in those with variant angina (28 +/- 14%) or syndrome X (25 +/- 13%). Concomitant determination of coronary blood flow showed significant (p < 0.001) decreases in those with variant angina (25 +/- 11%) and syndrome X (28 +/- 10%) but not in control patients (5 +/- 8%) or those with coronary artery disease (4 +/- 5%). Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin. CONCLUSIONS: These findings indicate that vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographically normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.

Relation of severity of symptoms to transient myocardial ischemia and prognosis in unstable angina.

OBJECTIVES: This study was undertaken to compare the relative power of the severity of angina versus that of any other clinical, electrocardiographic (ECG) and angiographic findings in predicting the risk of subsequent in-hospital coronary events in patients admitted to the coronary care unit for treatment of unstable angina. BACKGROUND: The presence or absence of chest pain has traditionally been used to guide management and therapy of unstable angina. However, recent studies raised the possibility that the cumulative duration of ischemia may be an additional index of prognosis. METHODS: We studied 104 consecutive patients admitted to the coronary care unit because of unstable angina. Diaries of symptoms were accurately kept. All patients underwent Holter ambulatory ECG monitoring during the 1st 24 h and angiography within 1 week of admission. RESULTS: During the hospital stay, 41 patients (group 1) had subsequent coronary events; the remaining 63 patients (group 2) had a good clinical outcome. Recurrence of chest pain after admission was observed in 76% of patients: 36 of the 41 group 1 patients (sensitivity 88%) and 43 of the 63 group 2 patients (specificity 32%). Anginal scores (frequency and persistence of pain, duration of each single episode and pain-free interval) showed high specificity but low sensitivity for detecting evolution toward subsequent coronary events. On Holter monitoring, the duration/24 h of the total number of ischemic episodes was consistently greater in group 1 than in group 2. A cumulative duration of ischemia > or = 60 min/24 h was observed in 34 of the 41 group 1 patients (sensitivity 83%) but in only 16 of the 63 group 2 patients (specificity 75%). High risk coronary artery lesions (left main coronary artery disease or complex stenosis) were detected in 36 of the 41 group 1 patients and in 26 of the 63 group 2 patients. CONCLUSIONS: Transient myocardial ischemia detected by Holter monitoring, but not chest pain, is the best predictor of unfavorable short-term clinical outcome. The decision to perform early angiography and revascularization cannot be based on symptoms alone.

Transient sympathovagal imbalance triggers "ischemic" sudden death in patients undergoing electrocardiographic Holter monitoring.

OBJECTIVES: The aim of this study was to investigate the relation between "ischemic" sudden death (arrhythmic death preceded by ST segment shift) and autonomic nervous system activity. Background. Mechanisms precipitating sudden death are poorly known despite the importance of detecting functional factors that may contribute to such a fatal event. METHODS: We analyzed the tapes of eight patients (seven men and one woman with a mean age of 66 +/- 8 years) who had ischemic sudden death during ambulatory electrocardiographic (Holter) monitoring. Four patients had unstable and four had stable angina; none was taking antiarrhythmic drugs. Twenty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computerized interactive Holter system. RESULTS: Five patients had ventricular tachyarrhythmias (ventricular fibrillation in three, ventricular tachycardia in two), and three had bradyarrhythmias (atrioventricular block in two, sinus arrest in one) as the terminal event; all eight patients showed ST segment shift (maximal change 0.46 +/- 0.16 mV; with ST elevation in two) that occurred 41 +/- 34 min (mean +/- SD) before sudden death. The standard deviation of normal RR intervals (SDNN) was 89 +/- 33 ms during the 10 +/- 6 h of Holter monitoring; 5 min before the onset of the fatal ST shift, SDNN measurements were significantly lower than during the initial 5-min period (48 +/- 10 vs. 29 +/- 9 ms; p=0.002). In control patients, the SDNN was 102 +/- 39 ms during Holter monitoring, whereas it measured 56 +/- 30 ms 5 min before the most significant episode of ST shift (p<0.01 vs. 29 +/- 9 ms [corrected] in the group with sudden death). CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These data suggest that sympathovagal imbalance may trigger fatal arrhythmias during acute myocardial ischemia, thus resulting in sudden death.

Myocardial ischemia induced by prostacyclin and iloprost.

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."

Comparison of verapamil versus propranolol therapy in syndrome X.

The effects of oral verapamil, 320 mg daily, propranolol, 120 to 160 mg daily, and placebo were compared in 16 patients presenting with transient myocardial ischemia without evidence of coronary atherosclerosis or vasospasm on angiography (syndrome X). Testing was done according to a randomized double-blind crossover placebo-controlled trial consisting of 3 consecutive 7-day treatment periods with verapamil or propranolol or placebo. Patients underwent continuous 48-hour electrocardiographic monitoring before therapy (run-in phase) and during the last 2 days of each treatment period. A total of 391 episodes of diagnostic (greater than or equal to 0.15 mV) ST depression was recorded during the trial. Of these, 23 were symptomatic. None of the episodes occurred while the patients were asleep, 25% during exercise, 35% during minimal physical activity and 40% at rest. Rest included activities demanding mental arousal (conversation, reading or watching television). Heart rate at the onset of ST depression was higher (greater than or equal to 10 beats/min) than that observed in the 5 minutes preceding ischemia in 95% of the episodes. In the group as a whole, the average number of ischemic episodes per 24 hours was significantly reduced during propranolol therapy compared with placebo (0.7 +/- 0.6 vs 3.9 +/- 1.8; p less than 0.0005). No significant differences were seen during verapamil treatment (3.4 +/- 1.7 vs 3.9 +/- 1.8). It is concluded that transient myocardial ischemia in syndrome X is mostly precipitated by an increase in oxygen consumption, presumably due to a heightened sympathetic activity. Accordingly, beta blockers may represent the first line of treatment.

Prognostic significance of silent myocardial ischemia in variant angina pectoris.

The present study investigates the prognostic significance of silent myocardial ischemia in variant angina. Forty-eight-hour Holter monitoring and coronary angiography were performed in 54 patients with transient ST elevation and no history of myocardial infarction admitted to the coronary care unit for worsening of symptoms. Coronary artery spasm was documented in most of these patients. Over the subsequent month, 20 patients (group 1) had a major coronary event (2 died, 6 had nonfatal myocardial infarction and 12 had urgent coronary revascularization), and the remaining 34 patients (group 2) had a good clinical outcome. From 2,578 hours of recording, 547 ischemic episodes were identified of which only 9% were associated with angina. The mean daily number of ST elevation in group 1 was similar to that in group 2 (4.8 +/- 5.1 vs 4.1 +/- 4.6; p = not significant). Conversely, the mean daily duration of such ischemic episodes was consistently greater in group 1 than in 2 (79 +/- 36 vs 37 +/- 25 minutes; p less than 0.005). The occurrence of greater than or equal to 1 long-lasting (greater than or equal to 10 minutes) episode of ST elevation was observed in 18 of 20 patients in group 1 (sensitivity 90%), but only in 4 of 34 in group 2 (specificity 88%). Significant coronary atherosclerosis (greater than 50% stenoses) was found at angiography in 18 of 20 patients in group 1, and in 18 of 34 in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of oral levodopa and carbidopa on coronary spasm in variant angina pectoris.

The effect of oral administration of 500 mg of levodopa with 50 mg of carbidopa, a peripheral dopadecarboxylase inhibitor, on coronary vasomotion during vasoconstrictor stimuli was examined in 15 patients with variant angina presenting with hyperventilation-induced myocardial ischemia. Patients were studied during 3 noninvasive sessions and 1 angiographic session. In all sessions the basic protocol consisted of provocation of coronary spasm by hyperventilation before and 2 hours after levodopa and carbidopa administration. During angiography, great cardiac vein blood flow, right atrial and aortic pressures were measured, and coronary angiograms were recorded at baseline and 1 to 4 minutes after each hyperventilation. Samples for dopamine plasma levels were drawn before and throughout the studies. In 3 selected patients, levodopa and carbidopa were associated with 30 mg of domperidone, an antagonist of dopamine peripheral receptors. Levodopa and carbidopa consistently prevented the occurrence of ischemia after hyperventilation in 6 of the 15 patients. This was due to inhibition of local coronary spasm in 2 patients and reduced coronary constriction in 4. Ischemia due to hyperventilation was still prevented despite addition of domperidone with levodopa and carbidopa. Plasma dopamine levels were 23 +/- 15 before and 739 +/- 284 pg/ml 2 hours after administration of levodopa and carbidopa. These findings are consistent with either a decreased central dopaminergic activity and associated disregulation of vasomotor tone, or a peripheral vasodilatory effect of increasing dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between plasma endothelin-1 levels and myocardial ischemia induced by exercise testing.

At peak exercise, plasma endothelin-1 concentration increases in patients with effort angina as well as thallium-201 radionuclide perfusion defects; the opposite occurs in patients with normal scans and in healthy volunteers. It is concluded that exercise-induced ischemia correlates with enhanced endothelin-1 production.

Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome.

Complex stenosis morphology frequently occurs in patients with unstable angina pectoris. However, its relation to transient myocardial ischemia and hospital outcome has not been ascertained. To address this issue, 88 patients with significant (greater than or equal to 50%) coronary artery disease presenting with angina--new onset (n = 38), worsening (n = 20) or at rest (n = 30)-were studied. Patients with left main artery disease, normal coronary arteries or occlusion of the ischemia-related arteries were not included in the study. Continuous electrocardiographic recordings were obtained during the first 24 hours. Angiography was performed within 1 week from admission. Complex morphology was defined as any stenosis with irregular borders, overhanging edges or intracoronary thrombus. Only data referring to the in-hospital outcome were considered in this study. Adverse end points were sudden death, myocardial infarction and emergency revascularization. Analysis of the angiograms revealed a complex morphology in 58 patients (group 1). The remaining 30 patients served as control subjects (group 2). Thirty-two of the 58 group 1 patients had an unfavorable clinical outcome (positive predictive value, 55%). A similar outcome occurred in only 2 of the 30 group 2 patients (negative predictive value, 93%). Of the 32 group 1 patients who had an unfavorable clinical outcome, 29 had a cumulative duration of transient myocardial ischemia of greater than or equal to 60 minutes per 24 hours. A similar duration of ischemia, however, was observed in another 6 group 1 and in 8 group 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of iloprost, a stable prostacyclin analog, on exercise capacity and platelet aggregation in stable angina pectoris.

The effects of iloprost, a chemically stable compound with prostacyclin mimetic activity, on exercise capacity and platelet aggregation were assessed in 24 patients with effort angina and proved critical (at least 70% diameter narrowing) coronary artery disease. Upright bicycle ergometer testing (25-W increments every 2 minutes) was performed during drug and placebo infusions using a crossover, randomized, single-blind protocol. Samples for measurements of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma were obtained in all patients before and during the study. Compared with placebo, intravenous iloprost consistently (p less than 0.001) prolonged exercise duration and time to onset of significant (0.1 mV) ST depression. Angina and ST depression occurred at a greater heart rate and rate-pressure product. Benefits were remarkable in some patients (67%) and not in others. Iloprost administration resulted in reduced platelet aggregation at peak exercise in all patients, whether they had consistent or little response to the drug. Thus, iloprost administration may improve exercise capacity in patients with stable exertional angina pectoris. Improvements are independent of changes in the major determinants of myocardial oxygen demand and associated with markedly reduced platelet aggregation, which may account for increased myocardial perfusion in patients with high sensitivity to coronary constriction.

Different susceptibility to myocardial ischemia provoked by hyperventilation and cold pressor test in exertional and variant angina pectoris.

Coronary constriction at the site of atherosclerotic stenoses has been suggested to play an important role in modulating the frequency of symptoms in patients with exertional angina. To investigate whether stimuli triggering coronary constriction have similar effects in patients with exertional and variant angina, responses to hyperventilation (HV) and cold pressor test (CPT) were evaluated. Twenty patients with chronic exertional angina, positive exercise test results and coronary heart disease were compared with 14 patients with variant angina and ST-segment elevation during an ergonovine test. In patients with exertional angina, the CPT produced diagnostic ST-segment depression in 6 of 20 patients (30%) at levels of rate-pressure product much lower than those during the exercise test; all patients had low effort tolerance and severe coronary artery disease. HV produced diagnostic ST-segment depression in only 1 of 20 patients (5%) (p less than 0.05 compared to that with CPT). Conversely, in patients with variant angina, HV produced ST-segment elevation in 11 of 14 patients (78%) and CPT produced elevation in only 2 of 14 (14%) (p less than 0.01). Thus, coronary constriction can provoke myocardial ischemia not only in patients with variant angina but also in some patients with exertional angina. Furthermore, the 2 groups of patients have a different susceptibility to stimuli known to produce coronary constriction.

Effects of iloprost (ZK 36374), a prostacyclin derivative, on platelet function after ischaemic exercise in patients with stable angina pectoris.

The effect of a chemically stable prostacyclin analogue (Iloprost) on platelet function was investigated in a controlled study in patients with angiographically confirmed stable angina pectoris after ischaemic exercise. In placebo experiments, ADP platelet aggregation was increased after exercise only when measured in whole blood and not in PRP. While plasma thromboxane B2 levels were unchanged, those of 6-keto PGF1 alpha were significantly although transiently increased after exercise. Iloprost displayed a potent antiaggregating activity in PRP and also reversed platelet hyperaggregation occurring in whole blood determinations after exercise. Plasma thromboxane B2 levels were significantly reduced but occasionally a rebound increase occurred 30 min. after end of the infusion. In contrast plasma level of 6-keto PGF1 alpha did not change after Iloprost and its recorded post-exercise increase was counteracted, thus suggesting a negative feed-back mechanism between Iloprost and natural prostacyclin. The data also suggest that degradation of the analogue is probably accomplished through pathways different from those of PGI2.

Studies on alkaline phosphatase isoenzymes in hepatic diseases. Relation to gamma-glutamyltransferase.

Isoenzymes of alkaline phosphatase (ALP) and total gamma-glutamyltransferase (gamma GT) have been studied in patients with increased total ALP. Fractionation of alkaline phosphatase yielded clinical information which could not be obtained by determination ALP and gamma GT alone. 1. There was a high degree of correlation between isoALP 1 (biliary band) and total gamma GT. 2. The ALP2 fraction increases after cytolysis in acute and chronic hepatitis. 3. A new ALP4 fraction appears, probably due to fibroblastic activity, in some histological types of cirrhosis.

Unstable angina: prognosis of the individual patient.

Not all patients diagnosed with unstable angina have the same outcome. Thus, it is incumbent on the physician caring for these patients to try to identify factors that will risk-stratify them. These factors include the degree of coronary angiographic stenosis, the lesion morphology, severity of symptoms, presence or absence of transient myocardial ischemia, and state of left ventricular function. In addition, many other factors including the patient's age, gender, and coexisting medical disorders must be considered when trying to prognosticate an individual patient. Clinical experience indicates that clinical indices that combine information provided by all of the above related variables should have more powerful prognostic significance than any individual variable.

Coronary hemodynamic effects of systemic thrombolysis in patients with unstable angina.

Intracoronary (i.c.) thrombus is a frequent finding in patients with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. To test this hypothesis, we studied 13 patients with active UA and ST-segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all patients 25 +/- 14 h after the last chest pain episode. Following angiography, patients received i.v. urokinase (UK: 1,000,000 IU/30 min); aortic pressure and GCVF were measured before and every 10 min following drug infusion, for a total time of 90 min. At baseline angiography, 5 of 13 patients (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 patients (Group 2) did not. Group analysis showed that UK increased GCVF and decreased anterior coronary resistance in Group 1 (respectively, from 86 +/- 33 to 114 +/- 41 ml/min: p less than 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml/min: p less than 0.05) but not in Group 2 (both: p = NS). In conclusion, UK has been shown to increase regional coronary blood flow in selected patients presenting with active UA, as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Changes in pulmonary hemodynamics predict benefits in exercise capacity after ACE inhibition in patients with mild to moderate congestive heart failure.

Several causes may affect the efficacy of angiotensin-converting enzyme (ACE) inhibitors in congestive heart failure (CHF). The present study was undertaken to identify what factors might predict benefits in exercise capacity after ACE inhibition in 22 patients with mild to moderate CHF. All patients underwent hemodynamic evaluation before and following an oral dose of quinapril (20 mg). They were then treated daily with 20 mg of quinapril and underwent exercise stress test off-drugs 1 day and 6 months later. Patients were grouped according to their relative changes in vascular resistances after quinapril: Group A (n = 15) showed a greater decrease in pulmonary vascular resistance (PVR) than in systemic vascular resistance (SVR) (% delta PVR/% delta SVR > 1). The opposite occurred in Group B (n = 7). Comparison of pretreatment baseline features revealed that the two groups had similar biochemical and hormonal variables, cardiac index, and SVR. Conversely, Group A patients had higher (p < 0.05) pulmonary artery pressure and PVR compared with Group B patients. Following quinapril, Group A patients showed a greater (p < 0.05) increase in cardiac index than Group B patients, despite a similar reduction in SVR. Accordingly, 1-day drug treatment significantly (p < 0.001) increased exercise duration in Group A (+29%), but not in Group B patients (+7%). Benefits in exercise capacity were still significant (p < 0.001) 6 months later.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypersensitivity of gastric parietal cells to selective H2-receptor stimulation in duodenal ulcer.

According to previous studies, duodenal ulcer patients not only secrete more acid than normal subjects, but are also more sensitive to pentagastrin stimulation. The aim of this study was to investigate whether hypersensitivity of parietal cells also occurs with specific H2-receptor agonists such as impromidine. Twelve duodenal ulcer patients and 12 healthy volunteers were admitted to the study. After 30 minutes of basal secretion, impromidine was infused at increasing doses (2.5; 5.0; 10.0; 20 micrograms/kg-1/h-1) in both groups of subjects. The gastric acid secretion was significantly higher in the duodenal ulcer group. The percentage, for each dose, of the calculated maximal response (CMR) was always higher in the patient group, and the difference with respect to the control group, was always higher in the patient group, and the difference, with respect to the control group, was statistically significant. Also, the average D50 was significantly lower in the duodenal ulcer group. Drug safety evaluation confirmed the presence of reversible dose-dependent pharmacological side effects. This study showed that parietal cells are more sensitive to highly selective H2-receptor agonists such as impromidine. These results add further information to the physiopathological features of duodenal ulcer.

[Exudative pericarditis with pleural plaques caused by exposure to asbestos, resolved with steroidal treatment]. / Pericardite essudativa associata a placche pleuriche da esposizione all'asbesto, risolta da trattamento steroideo.

We report a case of a 73-year old railwayman with an asymptomatic large pericardial effusion diagnosed by a routine echocardiogram. By clinical and laboratory tests we excluded an immune, infectious, tuberculous and neoplastic origin of the pericardial effusion. A computed tomography scan of the thorax showed left pleural plaques. Pleural and pericardial biopsies showed fibrohyaline plaques and diffuse aspecific, chronic inflammation consistent with asbestos exposure. By using steroid treatment there was no further evidence of pericardial inflammation or pericardial effusion at 8 month follow-up. Steroid drugs are therefore suggested as a first choice treatment in patients with pleuropericardial effusion as well as chronic asbestos exposure.

[Cardiological findings in acromegaly]. / Rilievi cardiologici nell'acromegalia.

Acromegaly involves cardiovascular complications mostly due to the presence of hypertension, diabetes and atherosclerosis. However the appearance of cardiac decompensation and arrhythmias in the absence of predisposing factors tends to support the hypothesis of a specific myocardiopathy caused by excess GH. In order to assess the existence and course of subclinical cardiac alterations, 8 acromegaly patients were examined: 4 males and 4 females aged 31-56 with GH levels of 24-70 ng/ml (M + CD X 47 +/- 16) and no cardiovascular symptoms. One of the patients had moderate hypertension and 2 reduced glucose tolerance. The basal ECG showed sporadic ventricular extrasystoles in 2 cases and alterations compatible with left ventricular hypertrophy in another, while the effort ECG produced an asymptomatic depression of the ST segment in the hypertensive patient. The chest X-ray was normal in all cases. The echocardiography study investigated: the thickness of the interventricular septum (IVS = 13.9 +/- 2.8 mm), the thickness of the posterior wall of the left ventricle (LPW = 10.6 +/- 2.9 mm), the septum/posterior wall ratio (IVS/LPW = 1.3 +/- 0.2 the diastolic diameter (DD = 15.4 +/- 11.4 mm), the fraction of shortening (FS = 39.1 +/- 14.5%), the ejection fraction (EF = 64.1 +/- 18.4%) and revealed asymmetrical septal hypertrophy in 3 cases, concentric hypertrophy in another two. In two cases the DD and EF were distinctly altered. The patients were re-examined 2-4 years after surgical or radiation treatment. GH levels (M +/- SD = 10.3 +/- 10.1 ng/ml) were normal in 4 cases and still high, though lower in another two. The remaining two patients had borderline GH levels with high Sm-C. The ECG and chest X-ray were unchanged while echocardiography revealed a significant deterioration in heart function as far as DD (56.4 +/- 10.8 mm, p less than 0.05) were concerned with frankly pathological results in 4 and 3 cases respectively. These data confirm the view that most acromegalic patients present subclinical abnormalities in cardiac function and that the evolution of these is slightly influenced by the reduction in GH and Sm-C. levels. In fact, while the persistence of high GH and Sm-C. levels may explain the progression of cardiac alterations in some cases, it does not in others. It is also emphasised that echocardiography appears to be the most sensitive non-invasive technique for the diagnosis and follow-up of cardiac involvement in acromegaly.

[Cardiac tamponade and rheumatoid arthritis: medical approach or pericardiectomy?]. / Tamponamento cardiaco e artrite reumatoide: approccio medico o pericardiectomia?

The authors report the case of a sixty-seven-year-old man with seronegative rheumatoid arthritis since 1967. After the treatment was discontinued, a symptomatic pericardial effusion developed during an exacerbation of rheumatoid arthritis. Histological findings suggested a rheumatoid origin. Consecutive pericardiocentesis and a concomitant adequate treatment resolved cardiac tamponade, at least during short-term follow-up. However, a long term observation will be necessary to exclude recurrent effusion or evolutive constrictive pericarditis.