Biomedical subjects
Publications and source records attributed to L Tavazzi.
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To determine the effects of a 6-month exercise training program on left ventricular (LV) function and remodeling, 49 consecutive patients (pts) with first Q anterior myocardial infarction (51 +/- 8 years), in I-II NYHA class, were studied 4 to 8 weeks after the acute episode and 6 months later by 2D-ECHO and upright bicycle ergometric test. At entry, pts were randomly allocated to physical training (T = 25pts) or control (C = 24pts). Global endocardial surface area (ESA), LV volumes and EF, extent of abnormal wall motion (%WMA), of regional dilatation (%REG DIL), and the shape distortion (DIST) index were analyzed. After 6 months, a significant increase in work capacity (4,589 +/- 1,417 to 5,379 +/- 1,485 KPM/min, p less than 0.03) and in lactic anaerobic threshold (45 +/- 13 to 63 +/- 15 W, p less than 0.01) was observed only in T. Initial ESA, EDV, EF, %WMA, %REG DIL, and DIST index were similar and they did not change after 6 months in both groups. However, pts with less than 40%EF had greater (p less than 0.0001) EDV and %WMA with marked DIST index at entry and showed further (p less than 0.01) deterioration after 6 months both in C and in T (EDV, ml/m2: 68 +/- 12 to 77 +/- 18 in C, 71 +/- 12 to 74 +/- 18 in T; %REG DIL: 39 +/- 20 to 49 +/- 24 in C, 32 +/- 12 to 35 +/- 23 in T; DIST index: 0.16 +/- 0.07 to 0.21 +/- 0.09 in C, 0.2 +/- 0.07 to 0.22 +/- 0.1 in T). These variables did not change in pts with greater than 40%EF. Thus, from these preliminary data, pts with less than 40%EF at entry are prone to further global and regional LV deterioration. Physical training does not seem to increase this spontaneous deterioration.
In this paper are reported the basal results of a multidisciplinary, multicenter study designed to explore in a population with ischemic disease the relation between hemostatic variables, conventional risk factors and atherothrombotic sequelae. 953 patients less than or equal to 69 yrs with documented coronary, cerebral or peripheral atherosclerotic disease were studied and followed-up for 24 months. Examinations included hemostatic and lipid laboratory assays, arterial Doppler examination, cerebral computerized tomography and nuclear magnetic resonance, exercise electrocardiogram and coronary angiography. Fibrinogen (301.4 +/- 71.52 mg/dl) correlated positively with antithrombin III (r = 0.27) and leukocytes (r = 0.25), negatively with HDL-cholesterol (r = 0.18) and tended to increase with smoking. Heavy smokers had higher leukocyte counts than non-smokers (8.0 +/- 2.0 vs. 7.2 +/- 2.1 x 10(3)/microliters), higher triglycerides (1.87 +/- 1.12 vs. 1.53 +/- 1.35 mmol/l) and lower HDL-cholesterol (0.93 +/- 0.27 vs. 1.00 +/- 0.25 mmol/l). FVII correlated positively with triglycerides (r = 0.16) and protein C (r = 0.45). vWF:Ag (145.4 +/- 70.58%) ad FVII:C (139.7 +/- 59.10%) were positively correlated (r = 0.44). FVIII:C correlated positively with fibrinogen (r = 0.21). Myocardial infarction survivors with associated cerebral and peripheral vascular lesions had higher FVIII:C, FVII, fibronogen and vWF:Ag. These findings suggest that hemostatic factors may enhance and/or mediate the effects of conventional risk factors in atherothrombotic ischemic events.
The aims of this study were to investigate the short-term haemodynamic changes occurring in post-infarct patients with left ventricular dysfunction undergoing a physical training programme and the prognostic implications of such changes. Ninety-five male patients with no evidence of congestive heart failure, consecutively admitted for exercise testing with haemodynamic monitoring in the supine position, in whom exercise pulmonary artery diastolic pressure (PAdP) exceeded 20 mmHg were enrolled in an in-hospital one-month physical training programme. After training all patients' exercise capacity increased by 24% (P less than 0.001) with no change of PAdP. At matched work load, heart rate decreased (126 +/- 21 vs 120 +/- 19 bt min-1, P less than 0.05) as did PAdP (27 +/- 5 vs 25 +/- 6 mmHg, P less than 0.05) and A-VO2 difference increased (9.5 +/- 1.7 vs 10 +/- 1.6 ml%, P less than 0.01). Similar results were observed in a subset of patients with exercise PAdP greater than 30 mmHg (30 patients). In 11 patients with inadequate cardiac output neither heart rate nor PAdP decreased after training and a disproportionate increase in blood pressure was noted. Clinical follow-up ranged from 1 to 8 years (62 +/- 32 months). Seven deaths, 12 reinfarctions and 14 coronary artery bypass graftings occurred. The modifications, after training in work capacity, heart rate and PAdP, were not predictive of events.(ABSTRACT TRUNCATED AT 250 WORDS)
We describe two cases of prolonged postischemic ventricular dilatation during myocardial scintigraphy with 99mTc MIBI, the new perfusion tracer that has only negligible redistribution. Ventricular dilatation, caused by true chamber dilatation and/or subendocardial ischemia, was still present over two hours after the induced ischemic episode, suggesting a prolonged duration of such a commonly believed fleeting scintigraphic finding.
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The purpose of the present study was to determine whether and to what extent mental stress can reproduce the perfusion defects that are known to be induced by exercise. Twenty-four patients with recent myocardial infarction (New York Heart Association functional class I) and evidence of ischemic response were evaluated by means of SESTAMIBI scintigraphy performed once after exercise and then again within 2 days after mental arithmetic. Baseline, exercise, and mental stress planar scintigrams were divided into 15 segments, and each segment was reviewed and scored on a scale of 0 to 3 by experienced observers using circumferential profile analysis. Conflicting scores were resolved by consensus. Electrocardiographic abnormalities were found in 15 of 24 patients during exercise and in none during mental arithmetic. Chest pain was experienced by five patients during exercise and by none during mental stress. Twenty patients showed reversible perfusion defects during mental stress. Of the 360 pooled scintigram segments, 99 evidenced uptake defects during exercise, and 48 of these showed the same defects during mental stress. Twenty of the remaining 51 of 99 segments were adjacent to segments showing reversible hypoperfusion, suggesting milder hypoperfusion in these segments during mental arithmetic than during exercise. Furthermore, 10 segments showed reversible defects only during mental stress such that seven of these occurred in areas adjacent to those that had shown exercise-induced reversible perfusion defects, two occurred in areas that had shown fixed SESTAMIBI defects during exercise, and one occurred in a segment that had shown completely normal uptake during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.
We studied the effects of experimentally induced emotional stress (mental arithmetic) on different hemodynamic parameters, catecholamine levels, and serum and platelet function tests in 25 postinfarction patients and in 10 apparently healthy, age-matched control subjects. Mental stress (10 minutes) induced significant increments in heart rate, systolic blood pressure, diastolic blood pressure, double product, and cardiac output, indicating a sympatho-adrenal stimulation that was confirmed by a significant increase in serum epinephrine and norepinephrine levels. All of the effects disappeared at minute 10 of recovery. Concomitantly, the test produced a significant increase in platelet aggregation (induced by 3 microM ADP or 1 microgram/ml collagen), the formation of circulating platelet aggregates, and an increase in thromboxane B2 levels in plasma and serum. These effects were also rapidly reversible. Similar activation of hemodynamic parameters and a similar but less evident increase in platelet function by emotional stress were observed in control subjects. A possible artifact due to factitious platelet activation by catheter sampling was excluded with experiments in which a 40-minute rest was introduced after the baseline period and before mental stress; platelet activation did not occur during baseline or rest periods, only after emotional stress. Furthermore, the antiplatelet drug dipyridamole reduced the stress-induced formation of platelet aggregates in postinfarction patients. These results demonstrate the existence of a direct link between emotional stress and platelet function and offer an explanation of one of the mechanisms through which mental stress may be involved in the development of coronary artery disease.
To assess the influence of mental stress on ventricular pump function in coronary patients, 88 postinfarction patients (mean age, 53 +/- 10 years) performed mental arithmetic during Swan-Ganz catheterization monitoring a mean of 44 +/- 16 days after myocardial infarction. The test lasted 3 minutes in 66 patients and 10 minutes in 22 patients. Two patients suffered acute pulmonary edema a few minutes after mental arithmetic, but no others complained of symptoms. Mean heart rate increased from 76 +/- 14 to 92 +/- 17 beats/min, mean systolic blood pressure increased from 138 +/- 22 to 160 +/- 27 mm Hg, mean diastolic blood pressure increased from 89 +/- 10 to 101 +/- 15 mm Hg, mean pulmonary wedge pressure increased from 13 +/- 6 to 19 +/- 8 mm Hg (p less than 0.001), and mean stroke volume decreased from 72 +/- 18 to 65 +/- 18 ml (p less than 0.001) during mental arithmetic. The changes in central hemodynamics during mental arithmetic were not predictable from noninvasive parameters. In the 22 patients who performed 10-minute mental arithmetic, the changes persisted throughout mental exercise. Eighty-one patients underwent supine bicycle ergometry after mental arithmetic: Absolute mental arithmetic-pulmonary wedge pressure values correlated with those during exercise at the first stage (25 W) (r = 0.63, p less than 0.001) and at maximal load (77 +/- 29 W) (r = 0.49, p less than 0.001), and pulmonary wedge pressure change between stress values and baseline during mental arithmetic did not correlate with those during the first stage of exercise (r = 0.09, p = NS) or during maximal load (r = 0.11, p = NS). Twenty-nine patients repeated the study 1 year after myocardial infarction, and the same hemodynamic changes were observed during mental arithmetic. In conclusion, it appears that mental stress can cause deteriorations of central hemodynamics that can be independent of changes in heart rate and blood pressure and are not predictable from exercise-induced changes; stress-induced cardiovascular activation can last for at least 10 minutes and is stable over long time periods.
To assess the effects of mental stress on left ventricular diastolic function in patients with congestive heart failure, nine patients aged 57 +/- 12 years with dilated cardiomyopathy (end-diastolic volume, more than 110 ml/m2; ejection fraction, less than 40%; mean, 28 +/- 8%) and congestive heart failure in New York Heart Association functional class II or III and 14 normal volunteers (mean age, 49 +/- 8 years) were studied during mental arithmetic lasting 10 minutes with echocardiographic Doppler monitoring of transmitral flow velocity. During mental arithmetic, the ratio of peak flow velocity in early versus late diastole (E/A) and deceleration time of early diastole did not change in normal controls. However, E/A increased significantly (from 1.6 +/- 1.5 to 1.9 +/- 1.7; p less than 0.01) and deceleration time markedly decreased (from 156 +/- 49 to 108 +/- 31 msec; p less than 0.001) in patients with congestive heart failure. In 16 postinfarct patients with ejection fraction of less than 40% studied during mental arithmetic with simultaneous hemodynamics and Doppler recordings, good correlations were found between pulmonary wedge pressure and Doppler parameters (wedge pressure versus E/A, r = 0.89; wedge pressure versus deceleration time, r = -0.87). During mental arithmetic, the pulmonary wedge pressure-E/A correlation was weaker (r = 0.67), whereas the correlation between pulmonary wedge pressure and deceleration time was stronger (r = 0.91). The value of 153 msec in deceleration time was the best cutoff point in predicting 12 mm Hg pulmonary wedge pressure, both at rest and during mental arithmetic: the higher the deceleration time, the lower the pulmonary wedge pressure, and vice versa. Among patients with congestive heart failure, five showed normal baseline deceleration time (195 +/- 21 msec; pattern 1), and the remaining four showed a short (less than 153 msec) deceleration time (108 +/- 13 msec; pattern 2). During mental arithmetic, deceleration time markedly decreased to as short as 119 +/- 20 msec in all patients except one with baseline pattern 1. Deceleration time further decreased to 75 +/- 6 msec in all patients with baseline pattern 2. Mental arithmetic induces changes in left ventricular diastolic function in patients with congestive heart failure. Transmitral echocardiographic Doppler provides a simple noninvasive method of estimating and monitoring pulmonary wedge pressure in patients with severe left ventricular dysfunction.
The psychophysiological responses to two mental stress tests (mental arithmetic and an interactive concentration task) were assessed in 168 unmedicated, male, postinfarction patients 36-69 years old. Patients also completed a standard battery of psychological tests. Psychophysiological responses were generally unrelated to age and education. Comparison of patients scoring high (more than 75%) and low (less than 25%) relative to the normal population on psychological measures indicated that heart rate and blood pressure responses to mental stress tests were significantly greater in those reporting low than in those reporting high neuroticism. The study population was subsequently divided into high, medium, and low cardiovascular responders on the basis of rate-pressure product reactions to the two stress tests. The three cardiovascular response groups did not differ in age, interval between myocardial infarction and stress testing, ejection fraction, incidence of exercise-induced ischemia, or ischemic signs during Holter monitoring. However, the high cardiovascular responders were more likely to manifest possible or definite electrocardiographic signs of ischemia or significant arrhythmia during mental stress testing than were the medium or low cardiovascular responders (50% versus 19.6% and 7%, respectively). High cardiovascular responders also reported lower levels of trait anxiety, neuroticism, psychophysiological symptoms, and depression.
We tested the hypothesis that psychological stress testing in the clinical laboratory provokes changes in the sympathetic and vagal activities regulating heart rate that can be assessed noninvasively using spectral analysis of RR variability. To account for the effects on respiration produced by talking, this study was performed with two different procedures: the I.K.T. (i.e., a computer-controlled mental task that is performed in silence and does not entail human confrontation) and a stressful interview. Finally, we assessed whether ischemic heart disease modifies the spectral changes induced by psychological stress by comparing a group of healthy subjects (age, 38 +/- 2 years) with a group of patients (age, 52 +/- 3 years) recovering from 1-month-old myocardial infarctions. The findings indicate that psychological stress induced marked changes in the sympathovagal balance, which moved toward sympathetic predominance. The low-frequency component of RR variability, a marker of sympathetic activity, increased from 58 +/- 5 normalized units (NU) to 68 +/- 3 NU with the I.K.T. and to 76 +/- 3 NU with the interview. This increase was absent in the group of post-myocardial infarction patients. However, arterial pressure increased significantly in both groups of subjects. The possibility of age playing an important role in determining the differences observed was disproved by the findings of a marked increase in low frequency with mental stimuli in an additional group of borderline hypertensive subjects with ages (55 +/- 2 years) comparable to those of post-myocardial infarction patients.
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Thrombolytic therapy has become an established procedure in patients with acute myocardial infarction (AMI). However, the aftercare of such patients is still uncertain. A meta-analysis of twenty trials of intravenous or subcutaneous heparin in AMI performed during the prethrombolysis period indicated a significant reduction in mortality, reinfarction, and stroke in treated patients. More recently, a study (SCATI) aimed at investigating the clinical effects of subcutaneous heparin (12.500 U two times daily) in the setting of thrombolytic therapeutical strategy in AMI, showed a lower in-hospital mortality, a trend towards lesser transient ischemic episodes in patients given streptokinase, and no difference in recurrent infarction rate. Ventricular thrombi were markedly reduced by heparin. Anti-platelet drugs were not permitted in the SCATI. In both GISSI 2 (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico) and International tissue plasminogen activator/streptokinase trials, aspirin was a recommended treatment, and subcutaneous heparin was randomized. No difference in mortality was noted in patients given heparin. In GISSI 2 recurrent ischemic episodes were also similar in treated and control groups, whereas embolic events were reduced by heparin. Major bleedings were rare in all trials. In conclusion, subcutaneous heparin is beneficial in AMI: however, the association with aspirin does not add consistent benefits. Heparin is effective in preventing thrombus formation and embolic complications - such effects are not shared by aspirin.
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