PubMed Health⌕ Search

Biomedical subjects

G A Lanza

Publications and source records attributed to G A Lanza.

At least 19 recordsLinked to original sources
PubMed2006

Cardiac syndrome X: a critical overview and future perspectives.

The classic definition of cardiac syndrome X (CSX) seems inadequate both for clinical and research purposes and should be replaced with one aimed at including a sufficiently homogeneous group of patients with the common plausible pathophysiological mechanism of coronary microvascular dysfunction. More specifically, CSX should be defined as a form of stable effort angina, which, according to careful diagnostic investigation, can reasonably be attributed to abnormalities in the coronary microvascular circulation.

Chest Pain↗
PubMed2005

Prognostic value of ventricular arrhythmias and heart rate variability in patients with unstable angina.

OBJECTIVES: To assess the prognostic value of ventricular arrhythmias (VA) and heart rate variability (HRV) in patients with unstable angina. DESIGN: Multicentre prospective study. SETTING: 17 cardiological centres in Italy. PATIENTS: 543 consecutive patients with unstable angina and preserved left ventricular function (ejection fraction >or=40%) enrolled in the SPAI (Stratificazione Prognostica dell'Angina Instabile) study. METHODS: Patients underwent 24 h ECG Holter monitoring within 24 h of hospital admission. Tested variables were frequent ventricular extrasystoles (>or=10/h), complex (that is, frequent or repetitive) VA, and bottom quartile values of time-domain and frequency-domain HRV variables. Primary end points were in-hospital and six-month total and cardiac deaths. RESULTS: Eight patients died in hospital (1.5%) and 32 (5.9%, 29 cardiac) during follow up. Both complex VA and frequent extrasystoles were strongly predictive of death in hospital and at follow up, even after adjustment for clinical (age, sex, cardiac risk factors and history of myocardial infarction) and laboratory (troponin I, C reactive protein and transient myocardial ischaemia on Holter monitoring) variables. At univariate analysis bottom quartile values of three HRV variables (standard deviation of RR intervals index, low-frequency amplitude and low to high frequency ratio) were associated with in-hospital death, and bottom quartile values of most HRV variables predicted six-month fatal events. At multivariate Cox survival analysis reduced low-frequency amplitude was consistently found to be independently associated with fatal end points. CONCLUSION: In patients with unstable angina with preserved myocardial function, both VA and HRV are independent predictors of in-hospital and medium-term mortality, suggesting that these factors should be taken into account in the risk stratification of these patients.

Aged↗
PubMed2004

Ethnic variations in acute coronary syndromes.

Although it is very likely that ethnic variations in the incidence and, possibly, clinical outcome of acute coronary artery disease events exist, the causes for such differences are many and difficult to address fully, given the complex interplay of contributing factors.

Acute Disease↗
PubMed2004

Diagnostic and prognostic value of ST segment depression limited to the recovery phase of exercise stress test.

OBJECTIVES: To investigate the diagnostic and prognostic value of ST segment depression limited to the recovery phase of an exercise stress test, as compared with that of ST segment depression appearing during exercise. SETTING: Exercise stress test laboratory of a university hospital. PATIENTS AND DESIGN: Clinical and angiographic data were compared for 574 consecutive patients who developed ST segment depression during the active phase of an exercise test (group 1) and for 79 patients who developed ST segment depression only during the recovery phase of the exercise test (group 2). RESULTS: There were no differences between the two groups in major clinical features. Significant coronary artery stenoses were found in 488 group 1 patients (85%) and in 62 group 2 patients (78%, p = 0.14). Three vessel or left main disease was found in 166 (29%) group 1 and in 14 (18%) group 2 patients (p = 0.045). At a median follow up of 55.3 months of 321 group 1 and 54 group 2 patients, there were no significant differences in major cardiac events between the groups (univariate relative risk 0.81, 95% confidence interval 0.25 to 2.68, p = 0.72). CONCLUSION: The diagnostic and prognostic power of ST segment depression limited to the recovery phase of an exercise test is largely similar to that of ST segment depression induced during effort; thus, assessing ST segment depression during recovery can significantly improve the clinical information derived from exercise stress tests.

Blood Pressure↗
PubMed2001

Low-grade exercise enhances platelet aggregability in patients with obstructive coronary disease independently of myocardial ischemia.

Moderate and strenuous exercise is known to enhance platelet aggregability in patients with obstructive coronary artery disease (CAD), but the effect of low-grade exercise is not known. We assessed shear-induced platelet aggregability before and after mild exercise (less than or equal to stage III of the modified Bruce protocol) in 27 patients with documented CAD who were receiving aspirin and in 12 subjects without CAD (controls). Ex vivo platelet aggregability was assessed in flowing whole blood as the time to occlude a collagen and adenosine diphosphate-coated ring; shorter times indicated greater aggregability. Aggregability, plasma von Willebrand factor (vWF) antigen, platelet and white cell counts, and hematocrit were measured at baseline, immediately after exercise (peak), and at 30 and 180 minutes after exercise. Exercise of similar workloads induced myocardial ischemia in 14 patients (group 1), but not in the other 13 (group 2) nor in controls. Both patient groups showed a reduction in aggregation time at peak exercise compared with baseline (group 1: 84+/-17 seconds at peak vs 96+/-22 seconds at baseline; group 2: 84+/-20 seconds at peak vs 99+/-20 seconds at baseline; p <0.03 for both comparisons), with a return to baseline values within 180 minutes. No significant variation occurred in controls (89+/-18 seconds at peak vs 85+/-21 second at baseline). Changes in vWF antigen did not differ significantly among groups. Aggregation times did not correlate with hematocrit or platelet and white cell counts. Thus, even low-grade exercise transiently enhances whole blood platelet aggregability in patients with obstructive CAD, but not in controls. The effect is independent of myocardial ischemia, occurs despite aspirin, and is likely dependent on hemodynamic factors interacting with coronary obstructions or dysfunctional endothelium.

Aged↗
PubMed2001

Platelet aggregability in cardiac syndrome X.

AIMS: To assess platelet aggregability at rest and in response to exercise in patients with cardiac syndrome X (anginal chest pain, ST-segment depression on exercise, angiographically normal coronary arteries). METHODS AND RESULTS: We performed a symptom/sign-limited exercise test in 31 patients with syndrome X, 25 patients with coronary artery disease and 29 healthy subjects. Platelet aggregability was measured in flowing whole blood at baseline, at peak exercise, and after 30 and 120 min, as the time to occlude a collagen/adenosine diphosphate coated ring (aggregation time). Resting aggregation time was shorter in syndrome X patients (83.2+/-12 s), compared to patients with coronary disease (94.0+/-18 s, P<0.01) and to healthy subjects (96.4+/-21 s, P<0.01). With exercise, aggregation time did not change in healthy controls, decreased in patients with coronary disease (-13.8 s at peak; 95% CI, -10.2, -17.3 s;P<0.001), but increased in syndrome X (+17.4 s 30 min after exercise; 95% CI, +10.4, +24.4 s;P<0.0001). The intravenous administration of an adenosine antagonist (theophylline) prevented the exercise-induced prolongation of aggregation time in syndrome X patients (n=11), but had no effect in healthy controls (n=11). CONCLUSION: Platelet aggregability at rest was increased in syndrome X patients, compared to patients with coronary artery disease and healthy subjects. In contrast to patients with coronary disease, however, platelet aggregability was reduced by exercise. This response was prevented by theophylline, strongly suggesting the involvement of adenosine.

Aged↗
PubMed2001

Impairment of cardiac autonomic function in patients with Duchenne muscular dystrophy: relationship to myocardial and respiratory function.

BACKGROUND: Previous studies reported an impairment of nervous autonomic activity in patients with Duchenne muscular dystrophy (DMD). However, the relationship of the autonomic dysfunction to the impairment of cardiac mechanical function and of respiratory failure is not completely understood. METHODS: We evaluated cardiac autonomic function by time- and frequency-domain heart rate variability (HRV) analysis on 24-hour Holter recordings in 60 patients with DMD (16.8 +/- 4.8 years) and 28 healthy control patients (15.2 +/- 4.6 years, P = not significant). The circadian rhythm of R-R interval, low frequency, high frequency, and low-frequency/high-frequency ratio was also assessed. In all patients, left ventricular ejection fraction was measured by 2D echocardiography; respiratory function was assessed by spirometry. RESULTS: All HRV parameters were lower in patients with DMD than in control subjects, with the percentage of differences between adjacent R-R intervals >50 ms (11.6% +/- 8.5% vs 27.3% +/- 14.1%, P =.00001) and high frequency (23.9 +/- 10.3 ms vs 36.1 +/- 12.2 ms, P =.0001) showing the strongest differences. A significant circadian rhythm of HRV variables was present in both groups, but it was considerably flattened in patients with DMD. There was no correlation between left ventricular ejection fraction and HRV indexes except for a weak correlation with high frequency (r = 0.30, P =.02) and with low-frequency to high-frequency ratio (r = -0.29, P <.03). Similarly modest correlations were found between forced vital capacity and high frequency (r = 0.4, P =.007) and low-frequency/high-frequency ratio (r = -0.32, P =.026). Multiple regression analysis did not show any independent predictive variable for the autonomic impairment. CONCLUSIONS: Our data show a marked impairment of cardiac autonomic function in patients with DMD, which appears to mainly involve the parasympathetic branch and appears to have a multifactorial origin.

Adolescent↗
PubMed2001

Spinal cord stimulation in patients with refractory anginal pain and normal coronary arteries.

BACKGROUND: Spinal cord stimulation (SCS) has been shown to be effective in patients with refractory angina and coronary artery disease. No previous study assessed the clinical effects of SCS in patients with refractory angina who present angiographically normal coronary arteries. METHODS: SCS was performed in 7 patients (4 men, 3 women, mean age 59.3 +/- 11 years) with refractory angina and normal coronary arteries. Clinical status was assessed 1 month after SCS device implantation and at a mean follow-up of 11 months (range 2-17 months) by: 1) an estimate of the number of anginal attacks and nitrate consumption in the 2 weeks prior to implantation and to follow-up visits; 2) a score of quality of life by a visual analogic scale; 3) a five-item questionnaire assessing effort angina and satisfaction with treatment; 4) treadmill exercise testing. RESULTS: At the last follow-up the number of anginal episodes (p < 0.001) and nitrate consumption (p < 0.004) were both reduced by SCS. Visual analogic scale score improved from 2.1 +/- 0.98 to 9.0 +/- 0.9 (p < 0.001) at 1 month and to 6.4 +/- 2.3 (p < 0.01) at the last follow-up. Questionnaire analysis showed that mild (p = 0.006) and moderate (p = 0.000) physical activity, as well as patient satisfaction with anginal status (p = 0.000) and with current treatment (p = 0.000) all improved by SCS. Finally, time to 1 mm ST segment depression, time to angina, and exercise duration were all prolonged by SCS. CONCLUSIONS: Our data point out that SCS may considerably improve anginal symptoms and exercise tolerance in a significant number of patients with refractory angina and normal coronary arteries and therefore it should be considered as a valuable treatment option in this group of patients.

Electric Stimulation Therapy↗
PubMed2000

Relationship between myocardial 123I-metaiodobenzylguanidine scintigraphic uptake and heart rate variability in patients with syndrome X.

BACKGROUND: We have recently demonstrated a striking impairment in cardiac uptake of 123I-metaiodobenzylguanidine (MIBG) in most patients with syndrome X. In this study we investigated the relationship between cardiac MIBG defects and cardiac autonomic activity in these patients. METHODS: MIBG myocardial scintigraphy and time-domain and frequency-domain heart rate variability (HRV) were compared in 11 syndrome X patients and 10 healthy controls. Cardiac MIBG uptake was assessed by the heart/mediastinum ratio and a cardiac MIBG uptake defect score (higher values = lower uptake). RESULTS: The heart/mediastinum ratio was lower (1.71 +/- 0.6 vs 2.19 +/- 0.3, p = 0.03) and MIBG uptake score higher (37.1 +/- 32 vs 4.0 +/- 2.5, p = 0.005) in syndrome X patients, whereas average HRV values did not differ between the two groups. However, while there were no correlations between MIBG uptake and HRV in controls, in syndrome X patients both the heart/mediastinum ratio and MIBG uptake score correlated significantly with two HRV parameters, specific for vagal activity: the square root of the mean squared differences of consecutive RR intervals (r = 0.73, p = 0.01, and r = -0.67, p = 0.02, respectively), and high frequency (r = 0.64, p = 0.03, and r = -0.74, p = 0.009, respectively). CONCLUSIONS; In patients with syndrome X, the impairment in cardiac MIBG uptake was associated with a reduction in HRV indexes mainly reflecting vagal modulation of sinus node, thus suggesting that a predominance of cardiac adrenergic activity may be present in those with abnormal cardiac MIBG scintigraphy.

3-Iodobenzylguanidine↗
PubMed2000

Prognostic role of heart rate variability in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: The aim of this study was to investigate whether heart rate variability may predict the outcome in patients with idiopathic dilated cardiomyopathy. METHODS: Time-domain and frequency-domain heart rate variability was analyzed on 24-hour Holter recordings of 56 patients with idiopathic dilated cardiomyopathy (70% males, mean age 49 +/- 16 years; left ventricular ejection fraction 28 +/- 6%). RESULTS: There were 8 cardiac deaths (14.3%) and 11 arrhythmic events (19.6%, either sudden death or sustained ventricular tachycardia) at a follow-up of 18.5 months (range 3-50 months). Furthermore, 6 patients were included in the list for cardiac transplantation, leading to a prevalence of total cardiac events of 37.5 % (21 patients). All time-domain and most frequency-domain heart rate variability parameters did not show any significant relationship with the end points. However, a low frequency to high frequency (LF/HF) ratio < 1.2 was associated with cardiac death (relative risk-RR 6.8, p < 0.03), arrhythmic events (RR 11.0, p < 0.004), and total cardiac events (RR 4.8, p < 0.002). On the multivariate Cox analysis, no variable showed an independent association with cardiac death, but an LF/HF ratio < 1.2 was the only variable independently predictive of arrhythmic events (RR 8.2, p < 0.02), and the most powerful predictor of total cardiac events (RR 3.8, p < 0.009). CONCLUSIONS: Our data show that, in patients with idiopathic dilated cardiomyopathy, a low LF/HF ratio, as assessed on 24-hour Holter recordings, is a powerful predictor of cardiac events.

Aged↗
PubMed1999

Effects of atrial pacing on arterial and coronary sinus endothelin-1 levels in syndrome X.

Syndrome X may be caused by a coronary microvascular dysfunction, possibly due to abnormalities in coronary endothelial function. Previous studies suggested that endothelin-1 (ET-1) might be involved in the pathogenesis of syndrome X. Baseline arterial and coronary sinus ET-1 levels were measured in 13 patients with syndrome X (10 women, 52+/-7 years) and in 8 control patients (5 women, 46+/-11 years). ET-1 was also measured after atrial pacing in 12 patients with syndrome X and all controls. To simultaneously assess the activity of nitric oxide, guanosine 3'-5'-cyclic monophosphate (cGMP) was also measured in 11 patients with syndrome X and 7 controls. Baseline arterial (2.27+/-0.46 vs. 1.90+/-0.22 pg/ml, p<0.05) and coronary sinus (2.03+/-0.43 vs. 1.68+/-0.28 pg/ml, p = 0.06) ET-1 plasma levels were higher in patients than in controls. After pacing, arterial ET-1 levels did not change in either group and coronary sinus ET-1 levels were also unchanged in controls. In contrast, coronary sinus ET-increased significantly in response to atrial pacing in patients with syndrome X (p = 0.023), and differences between coronary sinus ET-1 levels of patients with syndrome X and controls after pacing became highly significant (2.22+/-0.45 vs. 1.69+/-0.20 pg/ml, respectively, p = 0.006). No significant differences in arterial and coronary sinus cGMP concentrations were found between the 2 groups, both at baseline and after pacing. Our findings suggest that an increased vasoconstrictor activity of microvascular endothelium is present in at least some patients with syndrome X and may be involved in the pathogenesis of the syndrome.

Adult↗
PubMed1999

Atenolol versus amlodipine versus isosorbide-5-mononitrate on anginal symptoms in syndrome X.

The effects of a beta blocker (atenolol), a calcium antagonist (amlodipine), and a nitrate (isosorbide-5-mononitrate) on anginal symptoms in 10 patients with syndrome X were assessed in a crossover, double-blind, randomized trial. Only atenolol was found to significantly improve chest pain episodes, suggesting that it should be the preferred drug when starting pharmacologic treatment of patients with syndrome X.

Adrenergic beta-Antagonists↗
PubMed1999

Abnormal cardiac nerve function in syndrome X.

Syndrome X is likely to be caused by a dysfunction of small coronary arteries. Several authors suggested that an increased adrenergic activity could be involved in the pathogenesis of syndrome X, but studies investigating this topic by indirect methods led to conflicting results. We directly investigated cardiac sympathetic nerve function in syndrome X by myocardial radionuclide studies with 123I-metaiodobenzylguanidine (MIBG). Twelve syndrome X patients and 10 healthy controls were enrolled in the study. Cardiac MIBG uptake was assessed calculating the heart/mediastinum (H/M) ratio and a semiquantitative MIBG uptake score. Cardiac MIBG images were normal in all but 1 of controls (10%). Conversely, abnormalities in cardiac MIBG uptake were found in 9 syndrome X patients (75%, p < 0.01). In 5 patients the heart was totally or almost totally invisible on radionuclide MIBG images, while regional defects were found in other 4 patients. The H/M ratio was lower and cardiac MIBG uptake score strikingly higher in syndrome X patients. At 3 hours the H/M ratio was 1.70 +/- 0.6 in patients and 2.19 +/- 0.3 in controls (p = 0.03), while MIBG uptake score was 36.7 +/- 31 and 4.0 +/- 2.5 (p = 0.003) in the 4 groups, respectively. There were no differences between patients and controls in lung and salivary MIBG uptake. Reversible perfusion defects on stress thallium scintigraphy were found in 5 syndrome X patients (45%), all of whom also had abnormal MIBG scintigrams, while all 3 patients with normal MIBG scintigraphy also had normal thallium images. Thus, the function of efferent cardiac adrenergic nerve fibers is strongly impaired in the majority (i.e., 75%) of syndrome X patients. This abnormal function likely contributes significantly to the pathophysiologic and clinical features of syndrome X. We speculate that also the increased perception of cardiac pain reported in these patients could be an expression of the abnormal function of cardiac nerves, reflecting alterations of afferent nociceptive cardiac nerve fibers, as the abnormalities in MIBG uptake reflect alterations of efferent cardiac adrenergic nerve fibers.

3-Iodobenzylguanidine↗