Recurrent pericarditis.

Recurrent pericarditis is the most troublesome complication of pericarditis occurring in 15 to 30% of cases. The pathogenesis is often presumed to be immune-mediated although a specific rheumatologic diagnosis is commonly difficult to find. The clinical diagnosis is based on recurrent pericarditis chest pain and additional objective evidence of disease activity (e.g. pericardial rub, ECG changes, pericardial effusion, elevation of markers of inflammation, and/or imaging evidence of pericardial inflammation by CT or cardiac MR). The mainstay of medical therapy for recurrent pericarditis is aspirin or a non-steroidal anti-inflammatory drug (NSAID) plus colchicine. Second-line therapy is considered after failure of such treatments and it is generally based on low to moderate doses of corticosteroids (e.g. prednisone 0.2 to 0.5 mg/kg/day or equivalent) plus colchicine. More difficult cases are treated with combination of aspirin or NSAID, colchicine and corticosteroids. Refractory cases are managed by alternative medical options, including azathioprine, or intravenous human immunoglobulins or biological agents (e.g. anakinra). When all medical therapies fail, the last option may be surgical by pericardiectomy to be recommended in well-experienced centres. Despite a significant impairment of the quality of life, the most common forms of recurrent pericarditis (usually named as "idiopathic recurrent pericarditis" since without a well-defined etiological diagnosis) have good long-term outcomes with a negligible risk of developing constriction and rarely cardiac tamponade during follow-up. The present article reviews current knowledge on the definition, diagnosis, aetiology, therapy and prognosis of recurrent pericarditis with a focus on the more recent available literature.

Malignant pericardial effusion.

Malignant pericardial effusion is a common and serious manifestation in malignancies. The origins of the malignant process include solid tumors or hematological malignancies, while primary neoplasms of the pericardium are less common. In the oncological patient, pericardial effusion may develop by several different mechanisms, namely by direct or metastatic spread of the primary process or as a complication of antineoplastic therapies. In some cases, pericardial effusion may be the first manifestation of the disease, and that is why malignancy must be excluded in every case of an acute pericardial disease with cardiac tamponade at presentation, rapidly increasing pericardial effusion and an incessant or recurrent course. Thus, the definite differentiation of malignant pericardial effusion and rapid diagnosis are of particular therapeutic and prognostic importance. Management of these patients is multidisciplinary and requires team work, but at present there is a need for further research. An individual treatment plan should be established, taking into account cancer stage, the patient's prognosis, local availability and experience. In emergency cases with cardiac tamponade or significant effusion, initial relief can be obtained with pericardiocentesis. Despite the magnitude of this serious problem, little progress has been made in the treatment of pericardial effusion secondary to malignant disease.

Diagnostic issues in the clinical management of pericarditis.

AIMS: To review the current major diagnostic issues on the diagnosis of acute and recurrent pericarditis. METHODS: To review the current available evidence, we performed a through search of several evidence-based sources of information, including Cochrane Database of Systematic Reviews, Clinical Evidence, Evidence-based guidelines from National Guidelines Clearinghouse and a comprehensive Medline search with the MeSH terms 'pericarditis', 'etiology' and 'diagnosis'. RESULTS: The diagnosis of pericarditis is based on clinical criteria including symptoms, presence of specific physical findings (rubs), electrocardiographical changes and pericardial effusion. Although the aetiology may be varied, most cases are idiopathic or viral, even after an extensive diagnostic evaluation. In such cases, the course is often benign following anti-inflammatory treatment, and management would be not affected by a more precise diagnostic evaluation. A triage of pericarditis can be safely performed on the basis of the clinical and echocardiographical presentation. Specific diagnostic tests are not warranted if no specific aetiologies are suspected on the basis of the epidemiological background, history and presentation. High-risk features associated with specific aetiologies or complications include: fever > 38 degrees C, subacute onset, large pericardial effusion, cardiac tamponade, lack of response to aspirin or a NSAID. CONCLUSIONS: A targeted diagnostic evaluation is warranted in acute and recurrent pericarditis, with a specific aetiological search to rule out tuberculous, purulent or neoplastic pericarditis, as well as pericarditis related to a systemic disease, in selected patients according to the epidemiological background, presentation and clinical suspicion.

Management of heart failure in elderly people.

AIMS: To review currently available knowledge on presentation, clinical features and management of heart failure (HF) in elderly people. METHODS: To review currently available evidence, we performed a thorough search of several evidence-based sources of information, including Cochrane Database of Systematic Reviews, Clinical Evidence, Evidence-based guidelines from National Guidelines Clearinghouse and a comprehensive MEDLINE search with the MeSH terms: 'heart failure', 'elderly' and 'management'. RESULTS: A number of features of ageing may predispose elderly people to HF, and may impair the ability to respond to injuries. Another hallmark of elderly patients is the increasing prevalence of multiple coexisting chronic conditions and geriatric syndromes that may complicate the clinical presentation and evolution of HF. Although diagnosis may be challenging, because atypical symptoms and presentations are common, and comorbid conditions may mimic or complicate the clinical picture, diagnostic criteria do not change in elderly people. Drug treatment is not significantly different from that recommended in younger patients, and largely remains empiric, because clinical trials have generally excluded elderly people and patients with comorbid conditions. Disease management programmes may have the potential to reduce morbidity and mortality for patients with HF. CONCLUSIONS: Heart failure is the commonest reason for hospitalisation and readmission among older adults. HF shows peculiar features in elderly people, and is usually complicated by comorbidities, presenting a significant financial burden worldwide, nevertheless elderly people have been generally excluded from clinical trials, and thus management largely remains empiric and based on evidence from younger age groups.

Myopericarditis versus viral or idiopathic acute pericarditis.

OBJECTIVE: To investigate the relative incidence, clinical presentation and prognosis of myopericarditis among patients with idiopathic or viral acute pericarditis. DESIGN: Prospective observational clinical cohort study. SETTING: Two general hospitals from an urban area of 220 000 inhabitants. PATIENTS: 274 consecutive cases of idiopathic or viral acute pericarditis between January 2001 and June 2005. MAIN OUTCOME MEASURES: Relative prevalence of myopericarditis. Clinical features at presentation including echocardiographic data (ejection fraction (EF), wall motion score index (WMSI)) and follow-up data at 12 months including complications, results of echocardiography, electrocardiography and treadmill testing. RESULTS: Myopericarditis was recorded in 40/274 (14.6%) consecutive patients. At presentation, the following clinical features were independently associated with myopericarditis: arrhythmias (odds ratio (OR) = 17.6, 95% confidence interval (CI) 5.7 to 54.1; p<0.001), male gender (OR = 6.4, 95% CI 2.3 to 18.4; p = 0.01), age <40 years (OR = 6.1, 95% CI 2.2 to 16.9; p = 0.01), ST elevation (OR = 5.4, 95% CI 1.4 to 20.5; p = 0.013) and a recent febrile syndrome (OR = 2.8, 95% CI 1.1 to 7.7; p = 0.044). After 12 months' follow-up an increase of EF (basal EF 49.6 (5.1)% vs 12-month EF 59.1 (4.6)%; p<0.001) and decrease of WMSI (basal WMSI 1.19 (0.27) vs 12-month WMSI 1.02 (0.09); p<0.001) were recorded in patients with myopericarditis, with a normalisation of echocardiography, electrocardiography and treadmill testing in 98% of cases. Use of heparin or other anticoagulants (OR = 1.1, 95% CI 0.3 to 3.5; p = 0.918) and myopericarditis (OR = 2.3, 95% CI 0.7 to 7.6; p = 0.187) was not associated with an increased risk of cardiac tamponade or recurrences. CONCLUSIONS: Myopericarditis is relatively common and shows a benign evolution also in spontaneous cases not related to vaccination.

The changing face of infective endocarditis.

Infective endocarditis is a disease that continues to evolve in response to changing host conditions and other factors.

Omega-3 polyunsatured fatty acids role in postmyocardial infarction therapy.

Largely initiated by studies among Eskimos in the early 1970s, great attention has been given to possible effects of omega-3 polyunsatured fatty acids (PUFA) in cardiovascular diseases. A series of positive effects on pathogenetic mechanisms of cardiovascular disease has been discovered from laboratory studies in cell cultures, animal models and in humans. omega-3 PUFA can reduce platelets and leucocytes activities as well as plasma triglycerides. Moreover they can have antiarrhythmic properties. Nowadays patients who experienced myocardial infarction have decreased risk of total and cardiovascular mortality by treatment with omega-3 PUFA (1 g daily). This effect is present irrespective of high or low fish intake or simultaneous intake of other drugs for secondary prevention of coronary heart disease. Mainly on the basis of GISSI Prevention trial results, dietary supplementation with omega-3 PUFA is now recommended as a new component of secondary prevention after myocardial infarction in national and international guidelines.

GH-independent cardiotropic activities of hexarelin in patients with severe left ventricular dysfunction due to dilated and ischemic cardiomyopathy.

AIM: To investigate acute cardiotropic activities of hexarelin in patients with severe left ventricular dysfunction due to ischemic (iCMP) and dilated cardiomyopathy (dCMP). METHODS AND RESULTS: We studied the effect of intravenous hexarelin administration on growth hormone (GH) levels and left ventricular ejection fraction (LVEF) evaluated by radionuclide angiography in eight patients with dCMP (age 53.0+/-2.8, LVEF 16.7+/-2.1%) and five patients with iCMP (age 52.0+/-2.8 years, LVEF 22.6+/-2.1). Results were compared with a group of seven normal subjects (age 37.4+/-3.4 years, LVEF 64.0+/-1.5%) and seven patients with severe growth-hormone deficiency (GHD; age 42.0+/-4.4 years, LVEF 50.0+/-1.9%) previously studied with the same methodology. In dCMP and iCMP patients hexarelin induced a similar significant (P<0.05) increase in GH levels. In iCMP patients hexarelin induced a LVEF increase (peak LVEF 26.2+/-2.5%, P<0.05) as observed in normals and GHD, while in dCMP LVEF was unchanged (peak LVEF 17.7+/-1.7, P=NS). In all groups other hemodynamic parameters were unchanged. CONCLUSIONS: Acute hexarelin administration increases LVEF in iCMP patients (as in normals and GHD) but not in dCMP patients in spite of a similar GH releasing effect and basal LVEF. A possible explanation of the positive inotropic effect of hexarelin in iCMP could be a direct stimulation on viable myocardium or myocardial contractile reserve.

[Surgical treatment of atrial thrombosis. A transesophageal echocardiogram study]. / Trombosi atriale trattata chirurgicamente. Valutazione con ecocardiogramma transesofageo.

Transesophageal echocardiogram is the procedure of choice in the evaluation of masses located in the cardiac chambers. In this paper three cases of atrial thrombosis are presented: a) a free floating ball thrombus in the left atrium in a patient with moderate mitral stenosis; b) three thrombotic masses adherent to a central venous catheter; c) three thrombotic masses attached to Chiari s network in a patient operated for an ostium secundum atrial septal defect one year before. In all cases transesophageal echocardiogram has played a key role in the diagnosis. Medical therapy has been inadequate and so surgical removal has been performed. Unsuccessful medical therapy, a new episode of thrombosis, intracardiac permanent catheter infections and high risk of systemic and pulmonary embolism are indications for thrombectomy.

Role of lipid, apolipoprotein levels and apolipoprotein E genotype in young Italian patients with myocardial infarction.

BACKGROUND AND AIM: Studies of young patients with acute myocardial infarction (AMI) have demonstrated that conventional risk factors are usually responsible for their premature atherosclerosis. No account has yet been published of the risk profile of young Italians surviving an AMI. In this study, the conventional risk factors, lipids and apolipoproteins, and apolipoprotein E (APOE) allele distribution were evaluated in 98 consecutive AMI survivors (94 males, 4 females) aged 40.1 +/- 3.9 for at least three months after their acute event. These survivors were matched for age, sex, body mass index and presence of diabetes mellitus with 98 controls selected from subjects admitted to the same hospital for other reasons. METHODS AND RESULTS: Lipid profiles and APOE polymorphism were determined in both groups. Coronary angiography during hospitalization showed the absence of critical stenosis in 6.6% of the survivors, mono-vessel disease in 57.7%, and multi-vessel disease in 35.5%. The survivors had a higher frequency of smoking, hypertension, family history for coronary artery disease (CAD) and dyslipidemia, and a much greater frequency of 3 or more risk factors than the controls: Odd ratios (OR) 7.4, 95% confidence interval (CI) 2.5-18.6, p = 0.0000. Significant differences were found between the groups for triglycerides (p = 0.000002), total cholesterol (p = 0.003), LDL-cholesterol (p = 0.012), HDL-cholesterol (p = 0.0002), apolipoprotein AI (p = 0.00001), and Apolipoprotein B (p = 0.000001). No differences were observed in APOE allele distribution (APOE*4 0.11 vs 0.08, APOE*3 0.86 vs 0.89, APOE*2 0.03 vs 0.03), nor in lipid profile when both higher risk genotype (E3/4, E4/4, E2/4) and lower risk genotype groups (E2/2, E2/3, E3/3) were analysed. OR were calculated as measures of the association of the E4-positive genotypes with AMI. They indicated a non-significant increase in risk of AMI when the survivors were compared with the controls (OR 1.78, 95% CI 0.84-3.70, p = 0.13). CONCLUSIONS: This study provides further evidence that conventional coronary risk factors are usually present in young AMI patients. The APOE*4 allele was associated with a 1.8 non-significant increase in the risk of AMI in our group with premature CAD. Comparison with controls showed that the presence of three or more risk factors sharply increased the probability of premature CAD and that hyper-triglyceridemia is an independent risk factor. The data on APOE polymorphism are less certain and a larger study is needed.

Mitral valve prolapse. Comparison between valvular repair and replacement in severe mitral regurgitation.

BACKGROUND: The aim of this study was to analyse long term results of mitral valve repair of degenerative mitral regurgitation compared to valve replacement. METHODS: A hundred-twenty-five consecutive patients with severe mitral valve insufficiency who underwent cardiac surgery from January 1987 to December 1995 were included in the study. Mean age was 55+/-16 years (77 males, 48 females). Mitral repair was performed in 62 patients and mitral valve was replaced in 63 patients. Mean follow-up was 5 years. The repair procedures were based on quadrangular resection of the posterior leaflet, chordal replacement and transposition. Annuloplasty was performed in 100% of cases. The technique of valve replacement was conventional with complete excision of the valve in the majority of cases. RESULTS: Operative mortality following valve repair was 1.6%, no death occurred in the prosthesic group. In the repair group overall survival and re-operation rate were respectively 95.2% and 6.5%, while in the replacement group were 93.7% and 7.9%. No endocarditis and thromboembolic accidents were observed following valvuloplasty, while in the prostheses 6.3% of patients had endocarditis and 1.6% had a thromboembolic event. Mild or moderate left ventricular dysfunction was present in 5 patients after valvuloplasty and in 9 patients with prostheses. CONCLUSIONS: Considering these results we conclude that, in patients with severe degenerative mitral insufficiency, mitral valve repair is warranted whenever it is possible. The advantages given by maintaining the native valve suggest that surgery should be considered in asymptomatic patients before the occurrence of the left ventricular dysfunction.

Prognostic implications of detection of troponin I in patients with unstable angina pectoris.

In our study, troponin I was not a predictor of cardiac events and a negative troponin I test did not exclude the presence of severe coronary artery disease. A positive troponin I test in patients with unstable angina identified a subgroup with probable, more active coronary disease (with higher levels of C-reactive protein).

Clinical and epidemiological characteristics of juvenile myocardial infarction in Italy: the GISSI experience.

BACKGROUND: No clinical and epidemiological data are available about acute myocardial infarction (AMI) at a young age in large populations, due to the low prevalence of AMI in younger people. The aim of the present study is to analyze epidemiological and clinical characteristics of AMI among younger people in Italy, using the data bases of the three GISSI studies. METHODS: Analysis of epidemiological and clinical characteristics of AMI according to different age groups in the three GISSI studies that collected data from 1985 to 1993. RESULTS: In the GISSI-2 and GISSI-3 data bases, the prevalence of AMI at a young age (2 and 1.8% respectively; difference -0.2% with 95% CI from -0.4 to 0.3%), hospital mortality (2.3 and 1.9% respectively; difference -0.4% with 95% CI from -1.9 to 1.0%), and the rate of young female patients (8 and 7% respectively; difference -1% with 95% CI from -3.6 to 1.6%) are similar. In the GISSI-2 study, we observed that in comparison to elderly patients (> 70 years) young patients (< 40 years) are more frequently smokers (83.9 vs 21.0%; difference 62.9% with 95% CI from 58.5 to 67.3%) and have a higher rate of family history for CAD (42.1 vs 21.1%; difference 21.0% with 95% CI from 15.3 to 26.7%) and of hypercholesterolemia (28.3 vs 15.0%; difference 13.3% with 95% CI from 18.5 to 80.8%), but show a lower prevalence of hypertension (12.2 vs 44.3%; difference from -32.1% with 95% CI from -28.0 to -36.2%) and diabetes (2.9 vs 18.8%; difference -15.9% with 95% CI from -13.5 to -18.3%). AMI at a young age is generally the first event in ischemic heart disease; in comparison with older patients with previous AMI (6.4 vs 17.4%; difference -11.0% with 95% CI from -7.8 to -14.0%) and history of angina (23.2 vs 40.0%, difference -16.8% with 95% CI from -11.8 to -21.9%) this is less frequent. The rate of complications is lower in younger as opposed to older patients for both early (7.7 vs 31.2%; difference -23.5% with 95% CI from -20.0 to -26.9%) and late heart failure (2.9 vs 18.5%; difference -15.6% with 95% CI from -13.2 to -18.0%), as well as for angina (6.4 vs 10.5%; difference -4.1% with 95% CI from -1.1 to -7.1%), reinfarction (1.0 vs 3.3%; difference -2.3% with 95% Ci from -1.1 to -3.6%) and complete AV block (1.6 vs 6.6%; difference -5.0% with 95% CI from -3.3 to -6.7%). In young patients, we observed lower in-hospital (1.6 vs 21.1%; difference -19.5% with 95% CI to -21.6%) and six-month mortality (1.3 vs 8.1%; difference -6.8% with 95% CI from -5.0 to -8.5%). CONCLUSIONS: The incidence and mortality of AMI at a young age was steady during the period between 1988 and 1993. AMI at a young age is a clinical entity with specific characteristics that differ from those found in old patients. In addition, it has peculiar risk profile with a better short- and medium-term outcome.

Lack of relationship between the P1A1/P1A2 polymorphism of platelet glycoprotein IIIa and premature myocardial infarction.

BACKGROUND: The P1A1/P1A2 polymorphism of the platelet glycoprotein IIIa has been variably associated with an increased risk of coronary thrombosis. MATERIALS: We investigated the linkage between the P1A1/P1A2 polymorphism and the risk of myocardial infarction in 98 patients who suffered their first myocardial infarction at the age of 45 years or less and 98 well-matched control subjects without coronary artery disease. Lipid parameters were measured using conventional methods of clinical chemistry; P1A genotypes were determined by polymerase chain reaction and restriction enzyme digestion. RESULTS: There was no significant difference in the prevalence of P1A2-positive genotypes (either P1A1/P1A2 or P1A2/P1A2) between patients and control subjects (chi 2 = 0.66, d.f. = 1, P = 0.41). CONCLUSIONS: These results suggest that the P1A2 polymorphism of the platelet glycoprotein IIIa does not contribute to the genetic susceptibility to premature myocardial infarction.

[Differences in pharmacologic treatment after acute myocardial infarction. The role of treatment effectiveness]. / Differenze nel trattamento farmacologico dopo infarto miocardico acuto. Ruolo dell'efficacia dei trattamenti.

BACKGROUND: Despite growing interest concerning the prescription of different drugs in different clinical settings, no explanatory variables have been determined. The aim of this study was to verify if there are any differences in drug prescription at the time of hospital release following myocardial infarction and if any of these differences can be explained by scientific evidence concerning treatment efficacy. METHODS: All drugs prescribed to 430 patients discharged from three different cardiology departments after acute myocardial infarction were analyzed. Based on current scientific evidence, it has been, ascertained that aspirin, beta-blockers and ACE-inhibitors can be prescribed unless contraindicate whereas anticoagulants, nitrates and calcium antagonists should be prescribed only in specific clinical conditions. The odd ratio of prescription of each drug among the three cardiology departments was calculated and adjusted for any clinical and test result variables that can specifically affect drug prescription. RESULTS: Different clinical characteristics of the patients discharged from the three cardiology departments are the following: mean age ranges from 60 to 66 years (p < 0.001), the incidence of non-Q myocardial infarction ranges from 23 to 45% (p < 0.001), post infarction angina ranges from 6 to 15% (p = 0.016), left ventricular failure ranges from 6 to 13% (p = 0.003) and arrhythmia ranges from 5 to 18% (p = 0.007). The adjusted odd ratio for clinical and test results variables showed that prescriptions were similar for ACE-inhibitors (odd ratio 1.3; 95% confidence interval from 0.6 to 3.2), aspirin (OR 2.2; 95% confidence interval from 0.8 to 5.5), beta-blockers (OR 2.2, 95% confidence interval from 0.9 to 5.5) and oral anticoagulants (1.6; 95% confidence interval from 0.6 to 4.5). Instead, there is a statistically significant difference in the prescription of nitrates (OR 4.4; 95% confidence interval from 1.6 to 12.3) and of calcium antagonists (OR 5.4%, 95% confidence interval from 1.0 to 12.5). CONCLUSIONS: Evidence based drug efficacy after acute myocardial infarction seems to establish a uniform pattern of drug prescription in different cardiology departments.