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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 73 records · Page 4Linked to original sources
PubMed1999

Histologically proven myocarditis in patients with biventricular dysfunction and severe asymptomatic coronary artery disease.

The aim of our study was to investigate the pathogenesis of the global biventricular dysfunction observed in patients with critical coronary artery stenosis, but no evidence of myocardial ischemia or infarction. From January 1992 to January 1997, among consecutive patients undergoing invasive cardiac study including biventricular endomyocardial biopsy because of progressive heart failure (NYHA functional class III-IV) associated with biventricular dysfunction and no history of myocardial ischemic events, 7 patients had severe coronary artery disease (three vessel 4 patients; two vessel 1 patient, proximal occlusion of left anterior descending artery 2 patients). At two-dimensional echocardiography left and right ventricular end-diastolic diameter were 73 +/- 10.5 and 39 +/- 7 mm, respectively, left ventricular ejection fraction was 0.23 +/- 6.5 and right ventricular ejection fraction was 0.29 +/- 7.2. Histology showed extensive lymphocytic infiltrates with focal myocytolysis meeting the Dallas criteria for myocarditis in all patients. Two patients with active inflammation received prednisone and azathioprine in addition to conventional drug therapy for heart failure. At 6-month follow-up cardiac volume and function improved in immunosuppressed patients (left ventricular ejection fraction from 15 to 50% and from 20 to 38%, respectively) while they remained unchanged in conventionally treated patients. In conclusion, global biventricular dysfunction in patients with severe asymptomatic coronary artery disease and no evidence of previous myocardial infarction may be caused by myocarditis rather than by myocardial ischemia or hibernation.

Adult↗
PubMed1999

Additional predictive value of heart rate variability in high-risk patients surviving an acute myocardial infarction.

The aim of this study was to investigate the usefulness of heart rate variability (HRV) in predicting cardiac mortality in patients with a recent acute myocardial infarction at high risk of events. Time- and frequency-domain HRV was assessed on 24-hour pre-discharge Holter recording of 81 patients (mean age 65 +/- 10 years, 76.5% males) with 1) a recent acute myocardial infarction, and 2) left ventricular ejection fraction < 40% and/or a number of premature ventricular beats > or = 10/hour. There were 15 total cardiac deaths (18.5%) in a follow-up time of 29 +/- 15 months (range 6 to 48 months), with sudden death occurring in 11 patients (13.6%). Median values of low frequency (LF) were lower in patients with, compared to those without, total (p = 0.04) and sudden (p = 0.02) cardiac death. Similarly the low frequency/high frequency (LF/HF) ratio was lower in patients with fatal events (p = 0.03 and p = 0.02, respectively). Furthermore, mean of the standard deviations of all RR intervals for all 5-min segments < 20 ms, among time-domain variables, and very-low frequency (VLF) < 18 ms, among frequency-domain variables, significantly predicted cardiac death (relative risk-RR 2.94, p = 0.03; and RR 3.85, p < 0.005, respectively). Furthermore, VLF < 18 ms and LF/HF ratio < 1.05 significantly predicted the occurrence of sudden death (RR 3.52, p = 0.04; and RR 3.49, p = 0.04, respectively). Thus, our data show that HRV analysis is a useful tool for identifying patients with an actual increased risk of fatal cardiac events among patients who are basically considered at high risk according to the presence of an impaired left ventricular function and/or frequent ventricular arrhythmias.

Aged↗
PubMed1999

Homocysteine and arterial occlusive disease: a concise review.

Many cross-sectional and prospective studies have shown that raised serum/plasma levels of total homocysteine increase the risk of coronary, cerebral, and peripheral artery disease. The risk associated with hyperhomocysteinemia appears to be concentration-dependent and not attributable to traditional risk factors. The odds ratio for ischemic heart disease has been estimated to be 1.4 for every 5 mumol/l increase of total plasma homocysteine. Median fasting total plasma homocysteine in adult males is approximately 10 mumol/l. Mild hyperhomocysteinemia is estimated to occur in 5-10% of the general population. Plasma concentrations are increased as a result of age, male gender, impaired renal function, low vitamin B intake, and genetically-determined defects of the enzymes involved in homocysteine metabolism. Folate supplements can reduce total homocysteine levels by approximately 25%. Studies in vitro and in vivo indicate that homocysteine can impair endothelial function. Despite increasing recognition of hyperhomocysteinemia as a risk factor for arterial occlusive disease, irrefutable proof that mild hyperhomocysteinemia contributes directly to the pathogenesis of atherothrombosis will come if interventions to lower total homocysteine reduce cardiovascular events. Family studies may also provide evidence of causality if genetic causes of hyperhomocysteinemia are found to segregate with disease.

Arterial Occlusive Diseases↗
PubMed1999

In vitro hyperreactivity to lipopolysaccharide in patients with history of unstable angina is not associated with seropositivity for Cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae.

BACKGROUND: Inflammation and possibly chronic infections are associated with acute coronary syndromes; however, the mechanisms responsible for this association are not yet fully elucidated. The aim of this study was to assess whether the hyperreactivity of the inflammatory system, that we have shown in unstable patients with persistently elevated C-reactive protein and with recurrence of symptoms, was associated with chronic infection. METHODS: In 20 unstable angina patients seropositivity and antibody levels vs Cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae were measured and correlated with the interleukin-6 production in vivo in 1 ml of whole blood stimulated with 0.1 microgram lipopolysaccharide for 4 hours. RESULTS: No positive correlation was found between antibody titer and interleukin-6 levels. No correlation was also found between seropositivity to Cytomegalovirus, Helicobacter pylori or Chlamydia pneumoniae and interleukin-6 levels. CONCLUSIONS: Our study suggests that seropositivity for infective agents, including Chlamydia pneumoniae, does not affect the monocyte response to lipopolysaccharide and thus cannot account for the enhanced interleukin-6 production observed in unstable angina patients with raised levels of C-reactive protein and worse prognosis, and suggests the predominant role of the individual response to different stimuli.

Aged↗
PubMed1999

A simple assay for platelet-mediated hemostasis in flowing whole blood (PFA-100): reproducibility and effects of sex and age.

BACKGROUND: A simple assay for platelet-mediated hemostasis in flowing blood (PFA-100) has become available. Whole blood is aspirated through the central opening of a membrane coated with platelet agonists; the time required for a platelet thrombus to occlude the opening is defined as closure time; the shorter the closure time the greater the platelet aggregability. There are limited data on the normal range of values for this test, and the effects of sex and age are not known. The aim of this study was to determine the effects of sex and age on closure time in normal volunteers and to assess the reproducibility of the test in our laboratory. METHODS: Closure time using collagen/adenosine-5'-diphosphate was measured in 62 apparently healthy individuals 35 to 75 years of age (11 men and 17 women < 55 years and 22 men and 12 women > 55 years). RESULTS: Closure time was 96.6 +/- 24 s in men and 93.1 +/- 16 s in women (p = 0.20). In the entire group, closure time did not significantly correlate with age (r = -0.17, p = 0.18). However, men < 55 years tended to have a longer closure time than men > 55 years (109.7 +/- 23 vs 90.0 +/- 22 s, p = 0.08), whereas in women closure time was similar in those younger or older than 55 years (93.1 +/- 16 vs 93.3 +/- 18 s, respectively). In 20 samples tested in duplicate, the mean closure time was 80.9 +/- 10 s on the first determination and 81.5 +/- 12 s on the second (r = 0.89, p < 0.001). There was no significant correlation between closure time and hematocrit, platelet number, mean platelet volume, or leukocyte count. CONCLUSIONS: The platelet function analyzer PFA-100 showed a good reproducibility in apparently healthy subjects. No significant difference in closure time was found between men and women, nor between subjects younger or older than 55 years, although a tendency towards shorter values was found in older compared with younger men.

Adult↗
PubMed1999

Allelic polymorphism of the interleukin-1 receptor antagonist gene in patients with acute or stable presentation of ischemic heart disease.

BACKGROUND: One of the most potent pro-inflammatory mediators is the early-acting cytokine interleukin (IL)-1, whose actions are regulated by the structurally related IL-1 receptor antagonist (IL-1 Ra). IL-1 Ra is a competitive IL-1 inhibitor and a powerful anti-inflammatory agent. Several autoimmune and inflammatory diseases have been associated with an allelic polymorphism of the IL-1 Ra gene. METHODS: We investigated the frequency of allele 2 of an intron 2 polymorphism of the IL-1 Ra gene in 115 consecutive patients with ischemic heart disease -74 of which had a previous myocardial infarction (48 +/- 11 years), 21 chronic stable angina (54 +/- 10 years), and 20 unstable angina (54 +/- 9 years)--and in 80 healthy controls, matched for age and sex to patients with myocardial infarction (47 +/- 10 years). An 86 base pair variable tandem repeat in intron 2 of the IL-1 Ra gene was determined by a polymerase chain reaction-based method. RESULTS: The frequency of allele 2 was 15% in controls (carriage rate 25%) and 17% in ischemic heart disease patients (carriage rate 28%; p = 0.70). The allele 2 frequency did not differ significantly among the three patient groups. Among patients with myocardial infarction, the allele 2 frequency tended to be higher in patients with myocardial infarction < 40 years compared to those > or = 40 years (20 vs 11%, p = 0.20, OR 1.85, 95% CI 0.70-4.90), and in patients with C-reactive protein levels > or = 3 mg/l compared to those with values < 3 mg/l (31 vs 16%, p = 0.15, OR 2.38, 95% CI 0.64-9.25). CONCLUSIONS: These data do not show a clear-cut association between the allele 2 of this IL-1 Ra gene polymorphism and ischemic heart disease. Among patients with myocardial infarction, the increased allele 2 frequency in those of younger age and with higher levels of C-reactive protein merits further investigation.

Adult↗
PubMed1999

Circadian distribution of ischemic attacks and ischemia-related ventricular arrhythmias in patients with variant angina.

BACKGROUND: There are limited data about the circadian distribution of ischemic episodes in patients with variant angina. Furthermore, no previous study investigated whether ischemia-related ventricular arrhythmias follow a circadian variation in these patients. METHODS: The circadian variation of transient ischemia and ischemia-induced ventricular arrhythmias was assessed by cosinor methodology on 24-hour Holter recordings of 26 patients with variant angina. RESULTS: On the whole, 301 ischemic episodes were detected in the population, with premature ventricular complexes occurring in 49 of them (16%). Ischemic episodes followed a typical circadian variation (acrophase hr 02:36, p < 0.01) in the total sample. However, a significant circadian variation of ischemic episodes was detectable in the 14 patients without (n = 167, acrophase hr 04:00, p < 0.0001), but not in the 12 patients with (n = 134, p = 0.14) hemodynamically significant coronary stenoses, independently of the location (anterior/inferior) of ischemia. There was no significant circadian variation of ischemia-related ventricular arrhythmias. CONCLUSIONS: Among patients with variant angina, a clearcut circadian variation of ischemia is present in those without, but not in those with, hemodynamically significant coronary artery stenoses, thus suggesting that different pathophysiologic mechanisms may operate, at least in part, in triggering coronary spasm in these two subgroups of patients. There was no significant circadian variation of ischemia-related ventricular arrhythmias in these patients.

Angina Pectoris, Variant↗
PubMed1999

Preinfarction angina and improved reperfusion of the infarct-related artery.

Preinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of platelet-rich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrombotic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.

Angina Pectoris↗
PubMed1999

Acute coronary syndromes in women: pathophysiology and therapeutic options.

Patients presenting with acute coronary syndromes disclose a number of gender-related differences. Women are more likely than men to have unstable angina and less likely to present with myocardial infarction. Women have a better prognosis than men among patients with unstable angina. Among patients with myocardial infarction without ST-segment elevation, men and women show similar outcomes. In contrast, among patients with myocardial infarction and ST-segment elevation, women consistently show a worse prognosis than men. This difference is not fully explained by age, comorbidities, extent of epicardial artery disease, or baseline left ventricular function, and may reflect gender differences in pathophysiological, functional and anatomical variables. Moreover, revascularization procedures and several anti-ischemic drugs appear underutilized in women.

Acute Disease↗
PubMed1999

Circadianicity of hemostatic function and coronary vasomotion.

Acute myocardial infarction, sudden cardiac death and ischemic stroke show a circadian periodicity, occurring more frequently in the morning. Because arterial thrombosis is common to these disorders, a circadianicity of prothrombotic and antithrombotic processes may contribute to explain the 24 h rhythms of these acute events. Available data indeed indicate that coronary vasomotor tone, platelet aggregability, plasma inhibition of fibrinolysis, coagulant activity and blood viscosity are all greater in the morning than at other times of day, producting a relative prothrombotic state in the early morning.

Blood Coagulation↗
PubMed1998

Prognostic role of heart rate variability in patients with a recent acute myocardial infarction.

A low heart rate variability (HRV) has been shown to be a powerful predictor of cardiac events in patients surviving an acute myocardial infarction (MI), but it is not clear yet which among the HRV parameters has the best predictive value. Time domain and frequency domain HRV was assessed on 24-hour predischarge Holter recording of 239 patients with a recent MI. Patients were followed up for 6 to 54 months (median 28), during which 26 deaths (11%) occurred, 19 of which were cardiac in origin and 12 were sudden. Most HRVs did not show any difference between patients with or without mortality end points, but the average low-frequency and low-frequency/high-frequency ratio was lower in patients with events. However, when dichotomized according to cut points that maximized the risk of sudden death, several HRVs were significantly predictive of clinical end points. Overall, the mean of the standard deviations of all RR intervals for all 5-minute segments and the standard deviation of the mean RR intervals for all 5-minute segments were the time domain variables most significantly associated with mortality end points, whereas very low frequency was the most predictive frequency domain variable. Compared with the best time domain variables, very low frequency showed a better sensitivity (0.27 to 0.42 vs 0.19 to 0.33) for end points with only a small loss in specificity (0.92 vs 0.96). On multivariate Cox proportional analysis, a left ventricular ejection fraction <40% and a number of ventricular premature beats > or = 10/hour were the most powerful independent predictors for all end points, whereas no HRV was independently associated with the events. A low frequency/high frequency ratio < 1.05 only had a borderline association with sudden death (RR = 2.86, p = 0.076). Our data show a strong association between HRV and mortality in patients surviving a recent MI, with a slight better sensitivity of frequency domain analysis. In our study, however, HRV did not add independent prognostic information to more classic prognostic variables (e.g., left ventricular function and ventricular arrhythmias).

Aged↗
PubMed1998

Enhanced inflammatory response to coronary angioplasty in patients with severe unstable angina.

BACKGROUND: Systemic markers of inflammation have been found in unstable angina. Disruption of culprit coronary stenoses may cause a greater inflammatory response in patients with unstable than those with stable angina. We assessed the time course of C-reactive protein (CRP), serum amyloid A protein (SAA), and interleukin-6 (IL-6) after single-vessel PTCA in 30 patients with stable and 56 patients with unstable angina (protocol A). We also studied 12 patients with stable and 15 with unstable angina after diagnostic coronary angiography (protocol B). METHODS AND RESULTS: Peripheral blood samples were taken before and 6, 24, 48, and 72 hours after PTCA or angiography. In protocol A, baseline CRP, SAA, and IL-6 levels were normal in 87% of stable and 29% of unstable patients. After PTCA, CRP, SAA, and IL-6 did not change in stable patients and unstable patients with normal baseline levels but increased in unstable patients with raised baseline levels (all P<0.001). In protocol B, CRP, SAA, and IL-6 did not change in stable angina patients after angiography but increased in unstable angina patients (all P<0.05). Baseline CRP and SAA levels correlated with their peak values after PTCA and angiography (all P<0.001). CONCLUSIONS: Our data suggest that plaque rupture per se is not the main cause of the acute-phase protein increase in unstable angina and that increased baseline levels of acute-phase proteins are a marker of the hyperresponsiveness of the inflammatory system even to small stimuli. Thus, an enhanced inflammatory response to nonspecific stimuli may be involved in the pathogenesis of unstable angina.

Acute-Phase Proteins↗
PubMed1998

Incremental prognostic value of serum levels of troponin T and C-reactive protein on admission in patients with unstable angina pectoris.

Management of unstable angina is largely determined by symptoms, yet some symptomatic patients stabilize, whereas others develop myocardial infarction after waning of symptoms. Therefore, markers of short-term risk, available on admission, are needed. The value of 4 prognostic indicators available on admission (pain in the last 24 hours, electrocardiogram [ECG], troponin T, and C-reactive protein [CRP]), and of Holter monitoring available during the subsequent 24 hours was analyzed in 102 patients with Braunwald class IIIB unstable angina hospitalized in 4 centers. The patients were divided into 3 groups: group 1, 27 with pain during the last 24 hours and ischemic electrocardiographic changes; group 2, 45 with pain or electrocardiographic changes; group 3, 30 with neither pain nor electrocardiographic changes. Troponin T, CRP, ECG on admission, and Holter monitoring were analyzed blindly in the core laboratory. Fifteen patients developed myocardial infarction: 22% in group 1, 13% in group 2, and 10% in group 3. Twenty-eight patients underwent revascularization: 37% in group 1, 35% in group 2, and 7% in group 2 (p <0.01 between groups 1 or 2 vs group 3). Myocardial infarction was more frequent in patients with elevated troponin T (50% vs 9%, p=0.001) and elevated CRP (24% vs 4%, p= 0.01). Positive troponin T or CRP identified all myocardial infarctions in group 3. Only 1 of 46 patients with negative troponin T and CRP developed myocardial infarction. Among the indicators available on admission, multivariate analysis showed that troponin T (p=0.02) and CRP (p=0.04) were independently associated with myocardial infarction. Troponin T had the highest specificity (92%), and CRP the highest sensitivity (87%). Positive results on Holter monitoring were also associated with myocardial infarction (p=0.003), but when added to troponin T and CRP, increased specificity and positive predictive value by only 3%. Thus, in patients with class IIIB unstable angina, among data potentially available on admission, serum levels of troponin T and CRP have a significantly greater prognostic accuracy than symptoms and ECGs. Holter monitoring, available 24 hours later, adds no significant information.

Adult↗