[The ST and T in acute transient myocardial ischemia].
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Biomedical subjects
Publications and source records attributed to G Specchia.
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Left ventricular pseudoaneurysm is a rare condition which may develop after rupture of the ventricular myocardial wall. A localized hemopericardium confined is then formed outlined by the parietal pericardium. The pseudoaneurysmal sac is formed by clots and fibrous pericardial tissue and is directly connected to the ventricular chamber. There are no specific clinical signs to identify the disease. Two dimensional echocardiography and computerized tomography can allow the correct diagnosis to be made before cardiac catheterization. Two cases of left ventricular pseudoaneurysm occurring one after chest trauma and the other after acute myocardial infarction are reported.
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Peripheral lymphocyte adenosine deaminase (ADA) activity was assessed in a group of 31 patients with gynaecologic malignancies (19 with carcinoma of the portio, 7 with endometrial adenocarcinoma, 3 with ovarian cancer, 1 with adenocarcinoma of the cervix, 1 with liposarcoma myxoide). 30 female subjects, aged 30 to 70 years, were studied as the control group. Lymphocyte ADA activity in the 31 patients ranged from 0 to 7 U/10(7) cells with a mean of 2.3 U/10(7) cells (normal values: range 2-5 U/10(7) cells; mean 2.8 U/10(7) cells). In cases where the enzyme was absent or far below the controls, a faster evolution of the disease was observed. We would point out that lymphocyte ADA activity in the patients under investigations shows a broad range of variability. Our preliminary observations would suggest that lymphocyte ADA assessment in a larger series of cancer patients may add further prognostic informations.
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The behaviour of electrophoretic mobility (E.M.) of the blast cells has been investigated in 15 cases of acute non lymphoid leukemias (A.N.L.L.), (eleven cases of M1 type and four M5 type). The fast and homogeneous E.M. of M5 type in comparison with M1 has been underlined. E.M. of M1 blasts has been reported in a wide range varying from a "normal" migration (similar to that of normal neutrophils and monocytes) to a "fast" one (similar to M5 type). It is suggested that M1 leukemic forms, morphologically recognizable as the same leukemic type, are different L.A.N.L. indeed.
A mental arithmetic stress test was performed by 122 consecutive patients undergoing diagnostic coronary arteriography. Twenty-two patients showed significant ST segment abnormalities during the test (group 1). Of these patients, 20 performed a bicycle exercise test, which was positive in all of them. Seventy patients had a negative mental stress but a positive exercise test (group 2), whereas in 30 patients both tests were negative (group 3). There were no patients with a positive mental stress test and a negative exercise test. Mental stress induced a significant increase in heart rate and systolic blood pressure in the three groups of patients. Group 1 patients, however, achieved higher values of double product during mental stress and had a shorter exercise duration than group 2 and group 3 patients. The extent of coronary artery disease (CAD) was similar in groups 1 and 2, while group 3 patients had a significantly lower prevalence of two or more vessel disease. To investigate the pathogenetic mechanism of mental stress-induced myocardial ischemia, great cardiac vein flow was measured by means of the thermodilution technique in four patients with isolated left anterior descending artery disease, who showed ST segment depression in anterior leads in response to mental stress. In three patients without vasospastic angina the calculated coronary resistance decreased during mental stress, as a result of a normal vasodilatory response to the increased myocardial oxygen consumption induced by the test. By contrast, in one patient with variant angina, coronary resistance increased suggesting coronary vasoconstriction. Our findings demonstrate that mental arithmetic stress testing may induce significant ST segment abnormalities in patients with CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
Fifty male patients older than 65 years of age (mean 66.3) underwent a symptom-limited exercise test on an average of 34 days after acute myocardial infarction. After 4 weeks of supervised rehabilitation training and after one-year follow-up, the patients underwent controlled exercise tests. The ergometric parameters were compared with respective values in 10 healthy males (mean age 66.4, range 65-75). The rehabilitation training induced a substantial improvement in physical capacity (total work from 3149 +/- 1326 to 4791 +/- 1403 kg; P less than 0.001) with a better cardiovascular response: increased maximum oxygen pulse (from 8.97 +/- 2 to 10.7 +/- 2; P less than 0.001), decreased heart rate (from 120.5 +/- 16.1 to 111.3 +/- 14.7 beats min-1; P less than 0.05) and a decreased double product at a 75 W work load (from 22 866 +/- 4005 to 20 472 +/- 3982 beats min-1 mmHg; P less than 0.05). The recovery of physical capacity and cardiovascular tolerance in the physical exercise was nearly complete as compared with healthy subjects of the same age. During the training period one patient died from heart failure. In all the other patients the same improvement was still maintained one-year later. In conclusion, old age does not seem to be per se a contraindication to cardiac rehabilitation. Physiological beneficial effects from cardiac rehabilitation can also be received by patients older than 65 years of age.
We compared the effects of cold pressor test and mental stress on coronary hemodynamics in 16 patients with coronary artery disease. The patients were divided into 2 groups according to the clinical characteristics of chest pain. Group I included 5 patients complaining of angina at rest associated with transient ST-segment changes, while Group II comprised 11 patients with stable exertional angina. In all patients coronary arteriography disclosed a proximal left anterior descending artery disease. Thermodilution measurements of the great cardiac vein flow, the venous efflux from the territory supplied by the left anterior descending artery, were obtained during cold pressor test and, after return to control conditions, during a mental arithmetic stress, consisting of serial subtractions of a two-figure number from a four-figure number. Coronary resistance of the anterior region was calculated as the quotient of mean arterial pressure and the great cardiac vein flow. In both groups of patients heart rate, mean arterial pressure and the great cardiac vein flow increased significantly during cold pressor test as well as during mental stress. During cold pressor test, coronary resistance of the anterior region increased in all patients of Group I (p less than 0.05), but did not change significantly in Group II patients. During mental test, coronary resistance of the anterior region increased in 3 patients and decreased in 2 patients of Group I (p:NS), while a significant decrease in coronary resistance of the anterior region was found in all patients of Group II (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
The purpose of this study was to examine the clinical course of dilated (congestive) cardiomyopathy (DCM) and to identify the factors of prognostic significance. Between January 1969 and April 1982, 137 patients with a diagnosis of dilated cardiomyopathy were followed-up for a mean period of 48,7 +/- 40 months. Mean duration of illness before the first study was 15,5 months. A history of excessive alcohol intake was present in 22% of the patients and an influenza like syndrome in 9%. At diagnosis most of the patients were in NYHA functional class IV (43,5%) and III (35%). The 5-year survival rate was 45%, the mean annual mortality rate 10,2% and the highest mortality rate 14% in the second and third year. One hundred and seven patients (78%) progressed to major complications (worsening heart failure and death), while thirty patients (22%) showed stable or even improved conditions. Systemic or pulmonary emboli occurred in 18% of the patients, with a significant prevalence in patients with atrial fibrillation (p less than 0,05). Prognosis was unfavorably affected by the following factors: bi-ventricular heart failure as first clinical manifestation (p less than 0,01), intraventricular conduction delay (LBBB, LAHB) (p less than 0,05), significant cardiomegaly (cardiothoracic ratio greater than 0,53, p less than 0,001), left ventricular dysfunction (left ventricular fractional shortening less than 14%, p less than 0,005, left ventricular end-diastolic pressure greater than 17 mmHg, p less than 0,05, left ventricular end diastolic volume greater than 185 ml/m2, p less than 0,001, cardiac index less than 2,2/min/m2, p less than 0,001).
A retrospective study was conducted on 488 patients admitted in our rehabilitation center after a recent acute myocardial infarction. Purpose of the study was to assess the incidence and prognostic value of exertional hypotension in these patients. Of 488 patients admitted to the study 33 (6%) were found to have exertional hypotension; 14 patients had an inferior myocardial infarction, 18 patients had an anterior myocardial infarction, 3 patients had a history of previous myocardial infarction. In the follow-up period (28.3 +/- 13.2 months) the worse prognosis (death or pulmonary oedema) was associated with the presence during exercise of hypotension, ST segment elevation in leads were Q waves were present and no ST depression in other leads. In conclusion, recent anterior myocardial infarctions associated with hypotension and ST segment elevation during exercise appear to be at risk for future cardiac events.
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UNLABELLED: Detection of post-infarction left ventricular aneurysm may have important clinical and therapeutic consequences. Differences in selection and in diagnostic criteria account for the wide range of incidence of left ventricular aneurysm in angiographic and autopsy series. To assess the incidence and related pathological features of ventricular aneurysm, 410 consecutive patients were studied by two-dimensional echocardiography 3 to 8 weeks after the onset of an acute myocardial infarction. In 395 patients (96.3%) technically adequate echograms were obtained: 42 patients (10.6%) had evidence of left ventricular aneurysm defined as a well demarcated bulge in diastole and in systole with a thinned, a-diskinetic walls. The incidence rate of left ventricular aneurysm was 17% in 188 anterior myocardial infarctions, 1.9% in 157 inferior ones, 25.9% in 27 anterior plus inferior infarctions; ventricular aneurysms were not found in any of 15 lateral and 8 posterior myocardial infarctions. Aneurysms were apical or apical-anterior in 25 patients (59.5%), apical-septal in 8 (19%), apical-diaphragmatic in 3 (7.1%), apical-septal-diaphragmatic in 3 (7.1%) and postero-basal in 3 (7.1%). Intraaneurysmal thrombi were detected in 24 patients (57.1%). In 12 cases echograms showed pericardial effusion; this was more frequent (28.6%) than in patients without an aneurysm (7.9%; p less than 0.001). Among patients with an aneurysm, heart failure was present in 19 (45.2%), mitral regurgitation in 3 (7.1%), of systemic emboly in 4 (9.5%), severe ventricular arrhythmias in 4 (9.5%) and angina in 5 (11.9%). IN CONCLUSION: left ventricular aneurysm is a frequent early complication of myocardial infarction. Two-dimensional echocardiography provides non-invasive direct information on localization, extent and related pathological features of ventricular aneurysm and thus appears to be a useful screening technique.
353 patients enrolled in a cardiac rehabilitation program underwent a bicycle-ergometric test 28-60 days after an acute myocardial infarction. Twenty-nine patients (8.2%) had a previous history of chronic angina pectoris (more than 6 months before an acute myocardial infarction): 3 of these subjects did not develop myocardial ischemia after infarction; 26 (89.6%) (Group A) had an ischemic response on effort with horizontal or downsloping S-T segment depression of 2 mV. Ninety-four of 324 Patients without history of chronic angina pectoris had an ischemic response at exercise test (Group B) (p less than 0.001). In Group A the association of ischemic electrocardiographic changes and pain during the test was more frequent than in Group B (42.3% vs. 16%) p less than 0.01). During rehabilitation and follow up period (27.2 +/- 14 months) we observed that only 11.5% of Group A Patients remained symptomatic compared to 69.1% Group B Patients (p less than 0.001). In conclusion, a history of chronic pre-infarction angina pectoris appears to be a predictor of symptomatic ischemia after myocardial infarction.
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Acute lymphoblastic leukemia with hand-mirror cells (HMC) was diagnosed in nine adult patients. Blast HMC were seen only in the bone marrow (12-57% range). Cytochemical studies revealed a positive reaction to tartrate-sensitive acid phosphatase in the tail portion of the cells in seven cases, with a strong, localized cytoplasmic reaction in four. Leukemic cells lacked surface immunoglobulins and were E rosette negative in all cases. Normal levels of adenosine deaminase activity (ADA) were found in five of the seven patients. Electron microscope studies confirmed the hand-mirror shape of the cell. These HMC contained large numbers of mitochondria and microspikes in the handle portion of the cell. The patients failed to respond to initial conventional ALL chemotherapy, but the prolonged survival with passable health of the majority of these, despite their lack of complete remission, is emphasized.
Fifty-six patients with active Prinzmetal's variant angina were studied to determine the incidence and clinical significance of ventricular tachyarrhythmias and the correlation between arrhythmias and degree and time course of S-T segment changes during the ischemic attacks. Twenty-nine patients (Group I) had no ventricular arrhythmias in any of the 1,083 recorded episodes, while 27 patients (Group II) developed arrhythmias in 18% of the attacks. No significant differences in clinical, electrocardiographic, angiographic, or hemodynamic findings could be found between the 2 groups. In 23 of the 27 Group II patients, ventricular arrhythmias developed during maximal S-T segment elevation (occlusion arrhythmias), while in 10 they occurred during resolution of S-T segment changes (reperfusion arrhythmias); 6 of the latter patients also had occlusion arrhythmias. Eight of the 23 patients with occlusion arrhythmias and 6 of the 10 with reperfusion arrhythmias had ventricular fibrillation or ventricular tachycardia. Maximal S-T segment elevation was significantly greater (p less than 0.001) in patients with occlusion arrhythmias than in those without arrhythmias. The episodes with reperfusion arrhythmias were significantly longer (p less than 0.001) and showed a significantly greater S-T segment elevation (p less than 0.001) than those without arrhythmias in Group I patients. This study shows that significant ventricular tachyarrhythmias develop during ischemic attacks in about 50% of patients with active variant angina; clinical and angiographic features are not useful in distinguishing patients with arrhythmias from the others. Our findings suggest that in variant angina ventricular arrhythmias may be due to the effects of both coronary artery occlusion and reperfusion; both types of arrhythmias are correlated with the severity of ischemia, as measured by the degree of S-T segment elevation. Reperfusion arrhythmias also appear to be correlated with the duration of ischemia.