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Biomedical subjects

V Pasceri

Publications and source records attributed to V Pasceri.

33 records · Page 2Linked to original sources
PubMed1997

Usefulness of the addition of heart rate variability to Holter monitoring in predicting in-hospital cardiac events in patients with unstable angina pectoris.

Transient ischemia on Holter monitoring is a major determinant of outcome in unstable angina. In this study we investigated whether analysis of heart rate variability (HRV) may further improve the prognostic yield of Holter monitoring in this clinical setting. We performed 24-hour Holter monitoring in 75 patients with unstable angina (59 men, aged 62 +/- 9 years) within 12 hours of hospital admission. Number and duration of myocardial ischemic episodes, and both time domain and frequency domain HRV measures were obtained from Holter recordings. In-hospital major cardiac events (death or myocardial infarction) occurred in 7 patients (9%). Episodes of ST-segment depression on Holter monitoring were found in 6 of 7 patients (86%) with and in 26 of 68 patients (38%) without events (p <0.05). There were no differences between patients with or without events in both time domain (standard deviation [SD] of all normal RR intervals in the entire 24-hour electrocardiographic recording (SDNN), SD of the mean RR intervals for all 5-minute segments (SDANN-i), mean of SD of all RR intervals for all 5-minute segments (SDNN-i), percentage of differences between adjacent RR intervals >50 ms (pNN50), and square root of the mean squared differences of successive RR intervals) (RMSSD), and frequency domain (ultra low, very low, low, and high frequency) HRV indexes. However, the low-frequency/high-frequency (LF/HF) ratio was significantly higher in patients with cardiac events (2.12 +/- 1.4 vs 1.48 +/- 0.5, p = 0.01). Moreover, when considering only the 32 patients with myocardial ischemic episodes on Holter monitoring, the LF/HF ratio was again higher in the 6 patients with than the 26 patients without major cardiac events (2.45 +/- 1.5 vs 1.31 +/- 0.3, p <0.01). Multivariate logistic regression, including clinical and angiographic variables, showed that transient ischemia on Holter monitoring was the only independent determinant of outcome (odds ratio = 12.2, p = 0.03), with the LF/HF ratio being only slightly over statistical significance (odds ratio for 0.1 increments = 2.8, p = 0.08). Our data confirm that transient ischemia on Holter monitoring is a powerful predictor of cardiac events in unstable angina and indicates that an imbalance in cardiac autonomic tone toward a prevalence of sympathetic activity increases the risk of events in this group of patients.

Aged↗
PubMed1997

Cardiac autonomic function and sensitivity to pain in postmenopausal women with angina and normal coronary arteries.

An increased sensitivity to painful stimuli and an abnormal cardiac autonomic function have previously been reported in patients with angina and angiographically normal coronary arteries, a syndrome that mainly affects postmenopausal women. In this study we compared both general sensitivity to pain, by evaluating time to forearm ischemic pain (FIP) provoked by sphygmomanometer cuff inflation, and cardiac autonomic function, by measuring heart rate variability (HRV), and QT and QT(c) intervals on 24-hour Holter recordings, in 25 postmenopausal women with angina and normal coronary arteries and in 22 healthy postmenopausal women. Compared with controls, patients had a reproducible strikingly lower time to FIP (149 +/- 121 vs 295 +/- 158 seconds, p <0.001), whereas there were no differences between the 2 groups in HRV variables and mean 24-hour QT and QT(c) intervals. HRV indexes, and QT and QT(c) intervals also showed similar circadian patterns. Thus, our data show that postmenopausal women with angina and normal coronary arteries have an enhanced sensitivity to systemic painful stimuli, but no detectable impairment in cardiac autonomic function compared with a well-matched control group of postmenopausal healthy women.

Angina Pectoris↗
PubMed1997

Ischemic-like ST-segment changes during Holter monitoring in patients with angina pectoris and normal coronary arteries but negative exercise testing.

To evaluate whether Holter electrocardiographic monitoring may improve the detection of ST-segment depression in patients with anginal chest pain and normal coronary arteries, we performed symptom-limited exercise testing and 24-hour Holter monitoring in a group of 38 such patients (27 women, age 54 +/- 8 years). Patients were divided into 2 groups:group X1 included 28 patients with and group X2 10 patients without significant ST-segment depression during exercise testing. There were no significant differences between the 2 groups in age, gender, characteristics of chest pain, exercise duration, heart rate (HR), and blood pressure at peak exercise, but anginal pain during exercise testing was reported by 10 patients of group X1 (36%) and 9 of group X2 (90%) (p <0.01). Episodes of ST-segment depression on Holter monitoring were found in 17 patients of group X1 (61%) and in 5 patients of group X2 (50%) (p = NS). There were no differences between the 2 groups in daily number of ST episodes (3.6 +/- 4 vs 2.8 +/- 5 episodes per patient), symptomatic episodes (8% vs 18%), and duration of the episodes. On average, HR increased significantly, in a similar way, from 15 minutes before ST-segment depression to 1-mm ST in both groups, and its value at the onset of ischemia was similar in the 2 groups (102 +/- 22 vs 109 +/- 18 beats/min, p = NS). Finally, HR at 1-mm ST during Holter monitoring was significantly lower than that observed at 1-mm ST during exercise testing (127 +/- 16 beats/min, p < or = 0.01) in group X1, and it was also lower than that observed at peak exercise (136 +/- 22 beats/min, p < or = 0.01) in group X2. In conclusion, Holter monitoring can significantly increase the detection of ST-segment depression in patients with anginal pain and normal coronary arteries, indicating a cardiac, although not necessarily ischemic, origin of the pain. Indeed, 50% of our patients with negative symptom-limited exercise testing showed spontaneous ST changes, compatible with transient myocardial ischemia, during daily activities. Differences in the response of coronary microvascular tone to exercise testing and to stimuli operating during daily life are likely to play a significant role in determining these findings.

Activities of Daily Living↗
PubMed1997

Effects of bamiphylline on exercise testing in patients with syndrome X.

An abnormal stimulation of adenosine A1-receptors has been suggested to play a role in the pathogenesis of both chest pain and ischemia-like electrocardiographic changes in patients with syndrome X and a nonselective adenosine antagonist (theophylline) has been reported to be beneficial in these patients. In this study we investigated the acute effects of bamiphylline, a specific A1-receptor antagonist, in 16 patients with syndrome X (14 women, age 57 +/- 6 years), with both angina and ST-segment depression inducible during exercise testing. All patients underwent two treadmill exercise tests (Bruce modified protocol) on 2 separate days, 5 minutes after the end of randomized intravenous infusion of either placebo (saline solution) or bamiphylline (300 mg). Severity of chest pain was assessed by a 100 mm visual analogic scale. There were no significant differences in resting heart rate and blood pressure after bamiphylline or placebo. Rate-pressure product (20 600 +/- 5000 vs 20 200 +/- 5200 bpm.mmHg), time to 1 mm ST depression (549 +/- 196 vs 581 +/- 201 sec), time to angina (519 +/- 209 vs 571 +/- 196 sec), and exercise duration (717 +/- 134 vs 676 +/- 166 sec) were also not significantly different after bamiphylline or placebo, but there was a mild reduction of the severity of exercise-induced chest pain (30 +/- 22 vs 39 +/- 20 mm, p < 0.05) with the active drug. Thus, in patients with syndrome X, bamiphylline does not improve exercise-induced ST changes, suggesting that A1-receptors are not significantly involved in their appearance. In addition, bamiphylline had little effect on anginal pain, suggesting that this cannot be mediated exclusively by A1-receptor stimulation in these patients.

Angina Pectoris↗
PubMed1996

Autonomic changes associated with spontaneous coronary spasm in patients with variant angina.

OBJECTIVES: This study sought to investigate whether changes in nervous autonomic tone may have a role in the mechanisms triggering spontaneous coronary spasm in variant angina. BACKGROUND: Previous studies have suggested that both sympathetic and vagal activation may act as a trigger of epicardial artery spasm in patients with variant angina, but the actual role of autonomic changes in spontaneous coronary spasm remains unknown. METHODS: We analyzed the changes in heart rate variability associated with episodes of ST segment elevation detected on Holter monitoring in 23 patients with variant angina (18 men, 5 women; mean [+/-SD] age 59 +/- 12 years). For study purposes, episodes of transmural ischemia lasting > or = 3 min and without any ST segment changes in the previous 40 min were selected for analysis. Heart rate variability indexes were calculated at 2-min intervals, at 30,15,5 and 1 min before ST elevation and at peak ST segment elevation. Ninety-three of 239 total ischemic episodes (39%) fulfilled the inclusion criteria. RESULTS: The results showed that 1) high frequency (HF) (0.04 to 0.15 Hz), a heart rate variability index specific for vagal activity, decreased in the 2 min preceding ST segment elevation (p < 0.001) and returned to basal levels at peak ST segment elevation; 2) heart rate and low frequency (0.04 to 0.15 Hz), which are partially correlated with sympathetic activity, showed a significant increase at peak ST segment elevation (p < 0.001 for both); 3) the pattern of the HF reduction before ST segment elevation was consistently confirmed in several subgroups of ischemic episodes, including those of patients with or without coronary stenoses, those of patients with anterior or inferior ST segment elevation, those occurring during daily or nightly hours and silent episodes. There were no significant variations in heart rate variability in control periods selected from Holter tapes of patients and before ST segment elevation induced by balloon inflation in 20 patients undergoing coronary angioplasty. CONCLUSIONS: Our data show that changes in autonomic tone are likely to contribute to trigger or predispose to epicardial spasm. In particular, although not excluding an active role for adrenergic mechanisms, our data suggest that a vagal withdrawal may often be a component of the mechanisms leading to spontaneous coronary vasospasm.

Aged↗
PubMed1996

Preconditioning by transient myocardial ischemia confers protection against ischemia-induced ventricular arrhythmias in variant angina.

BACKGROUND: In experimental models, ischemic preconditioning of the heart protects against ischemic damage and ventricular arrhythmias during subsequent coronary occlusion. In this study, we investigated whether protection against ischemic suffering and ischemia-induced arrhythmias may occur after spontaneous transmural ischemia in humans. METHODS AND RESULTS: We performed 24-hour Holter monitoring in 10 patients with variant angina who developed complex ventricular arrhythmias (CVAs, more than five premature ventricular beats per minute or repetitive ventricular arrhythmias) during episodes of ST-segment elevation. A total of 150 episodes of ST-segment elevation were detected on Holter monitoring, 21 (14%) of which showed CVAs. Episodes separated from the previous one by a time interval of < or = 30 minutes or by a time interval of > 30 minutes did not differ in either magnitude or duration of ST-segment elevation, but CVAs occurred more frequently in the second group (3% versus 29%, P < .0001). The time interval from the preceding ischemic episode was longer for the episodes with compared with those without CVAs (197 +/- 275 versus 57 +/- 87 minutes, P < .001), but these two groups of episodes also had similar severities and durations of ST-segment elevation. Finally, when we analyzed 13 clusters of two to six ischemic episodes, CVAs were found much more frequently in the first (92%) than in the last (23%, P = .009) episode of the clusters, while ST-segment elevations were similar (2.1 +/- 1.6 versus 2.2 +/- 1.1 mm) and ischemia durations shorter in the first than in the last episode (3.9 +/- 3.6 versus 6.1 +/- 1.7 minutes, P = .03). CONCLUSIONS: Our data indicate that preconditioning by transient ischemia induces a significant protection against ischemia-induced CVAs in patients with variant angina. This beneficial effect was not related to a reduction in either severity or duration of ischemia, suggesting that arrhythmic protection was a direct consequence of preconditioning rather than an epiphenomenon of ischemic protection.

Aged↗
PubMed1996

Preinfarction angina as a predictor of more rapid coronary thrombolysis in patients with acute myocardial infarction.

BACKGROUND: When a myocardial infarction is preceded by angina, the infarct tends to be smaller than when there is no preinfarction angina. Prompt recanalization of the occluded infarct-related artery is crucial in limiting the size of the infarct. We prospectively studied the relation among preinfarction unstable angina, the speed of coronary reperfusion, and the size of the infarct in patients with acute myocardial infarction receiving thrombolytic therapy. METHODS: We compared 14 patients who had unstable angina during the week before myocardial infarction with 9 patients who had no preinfarction angina. Coronary arteriograms were obtained at base line and 15, 35, 55, and 90 minutes and 24 hours after the start of thrombolytic therapy. The size of the infarct was estimated on the basis of creatine kinase and creatine kinase MB levels, which were measured every 4 hours during the first 24 hours. RESULTS: Complete reperfusion (a flow of grade 3 according to the Thrombolysis in Myocardial Infarction classification) was achieved at 35 minutes in 64 percent of the patients with preinfarction angina but in none of those without preinfarction angina (P = 0.006); at 55 minutes in 86 percent and 38 percent, respectively (P = 0.05); and at 90 minutes in 86 percent and 50 percent, respectively (P = 0.14). The mean (+/- SD) time to reperfusion was 27 +/- 16 minutes in the group with preinfarction angina and 48 +/- 17 minutes in the group without preinfarction angina (P = 0.04); the peak creatine kinase levels were 1118 +/- 783 and 2395 +/- 1615 U per liter, respectively (P = 0.03); the peak creatine kinase MB levels were 102 +/- 67 and 251 +/- 186 U per liter, respectively (P = 0.009); and the 24-hour integrated creatine kinase MB levels were 1716 +/- 1171 and 4267 +/- 3252 U.liter-1 x 24 hours, respectively (P = 0.009). The time to reperfusion was positively correlated with the indexes of infarct size (r > or = 0.53, P < or = 0.02). CONCLUSIONS: In patients with acute myocardial infarction preceded by unstable angina, as compared with those without preinfarction angina, thrombolytic therapy resulted in more rapid reperfusion and smaller infarcts. Earlier myocardial reperfusion may thus account for the smaller infarct size in patients with preinfarction angina.

Adult↗
PubMed1996

Clinical markers of thrombolytic success.

Although a number of markers of successful coronary thrombolysis have been proposed, only a few of these have the two necessary features of a clinically useful marker: (1) widespread early availability and (2) good predictive value. The reduction in ST-segment elevation on the standard 12 lead electrocardiogram 1-4 h after initiation of thrombolysis may be the simplest and most useful clinical 'tool' to gauge the effectiveness of thrombolytic therapy. The predictive value of this single marker might be further improved by combining it with assessment of the rate of increase of serum myoglobin and of troponin T, provided these determinations were rapidly available.

Biomarkers↗
PubMed1996

Expanding concepts in ischaemic heart disease: implications for clinical practice and research.

In the late Eighties, a series of observations from several institutions around the world has dramatically revolutionized the traditional notion that the occurrence of myocardial infarction was related most of the time to the development of critical flow-limiting coronary stenosis. All these studies showed that the infarct-related artery had only minimal or mild stenosis in about two thirds of the cases. Therefore, contrary to our previous beliefs, in clinical practice the detection of coronary stenosis has a lesser role in the prognostic assessment of patients with ischaemic heart disease, unless associated with extensive ischemia or with phases of instability. In fact, the major determinants of prognosis are represented by age, left ventricular function, effort tolerance and especially by the clinical stability or instability of angina. According to the Bayesian an theorem, in low risk patients any diagnostic test has a very low predictive accuracy, unless very high specificity criteria are used. The value of diagnostic tests in the assessment of patients' prognosis should be evaluated in intermediate risk groups. The emphasis of clinical research has, therefore, shifted from the detection of flow-limiting stenosis to the study of the multiple and varied dynamic causes of stable and unstable ischaemia, where the possibilities of making new, seminal observations are greater.

Aged↗
PubMed1995

Relation between myocardial infarction site and pain location in Q-wave acute myocardial infarction.

Location, severity, duration, and time course of pain were assessed in 104 consecutive patients with either first or second, anterior or inferior Q-wave acute myocardial infarction (AMI). Pain severity was assessed using a visual analog scale. Pain location and radiation were similar in 48 patients with anterior and 56 patients with inferior wall AMI. Pain duration (6.1 +/- 6.4 vs 6.5 +/- 5.4 hours, p = NS) and severity (68 +/- 21 vs 61 +/- 21 mm, p = NS) were also similar. The pain was continuous in 34 patients with anterior (71%) and in 42 with inferior (75%) wall AMI. Among the 41 patients who did not receive thrombolytic therapy, 18 patients with continuous pain had a higher creatine kinase peak level than the remaining 23 patients with intermittent pain or preinfarction angina, or both (2,065 +/- 1,017 vs 1,162 +/- 994 IU, p < 0.01). The incidence of gastrointestinal symptoms was slightly higher in patients with inferior than anterior wall AMI (70% vs 48%, p < 0.05). Among 32 patients admitted with a second AMI, pain location was similar in 14 who had both infarcts in the same myocardial region, but was different in 12 of 18 (67%) who had a first and second infarct in different regions (p < 0.001). Thus, patients with anterior or inferior wall AMI experienced pain in similar body regions. However, in patients who presented with > 1 AMI, different locations of the infarction pain were highly predictive of ischemia occurring in different myocardial regions. Finally, patients with preinfarction angina or intermittent pain tended to have smaller infarcts.

Adult↗
PubMedDate not supplied

Helicobacter pylori is an aetiological factor for ischaemic heart disease: the case against.

Helicobacter pylori is one of four organisms often investigated for ari association with ischaemic heart disease. The four, including Chlamydia pneumoniae, Cytomegalovirus and Herpes virus, cause low-grade, life-long infections that can produce a persistent inflammation, the kind that leads to heart disease. Several studies suggest an association, but others suggest none. Patients with poor access to medical care are more likely to become infected and also more likely to suffer from coronary artery disease. Although the literature data are provocative and interesting, the two things may not be related. Helicobacter pylori infection is quite prevalent among individuals without ischaemic heart disease and absent in many of those with ischaemic heart disease. Thus, more definite answers about whether there is any link between Helicobacter pylori and cardiovascular disease are needed. It would be essential to establish the specific mechanisms that possibly confer vulnerability or protection toward coronaropathy. But a definite answer could come from clinical trials designed to test whether antibiotics can prevent the disease. Until now, no randomised trial has suggested a positive effect of Helicobacter pylori eradication in reducing the incidence of cardiac events.

Global Health↗