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.

Acute myocardial infarction in young adults: prognostic role of angiotensin-converting enzyme, angiotensin II type I receptor, apolipoprotein E, endothelial constitutive nitric oxide synthase, and glycoprotein IIIa genetic polymorphisms at medium-term follow-up.

BACKGROUND: A number of reports have investigated the association between various gene polymorphisms and the phenotypic expression of myocardial infarction. No investigations have evaluated the prognostic role of genetic factors in young people with premature coronary disease. The aim of this study was to investigate the influence of genetic factors compared with that of conventional risk factors on follow-up events in a population of Italian young adults with myocardial infarction. METHODS AND RESULTS: The study population consisted of 106 young patients (mean age 40 +/- 4 years, range 23 to 45 years) with diagnosis of acute myocardial infarction. Clinical and genetic data from the group of patients with events during follow-up were compared with those from patients without events. The following genetic polymorphisms were tested: angiotensin I converting enzyme, angiotensin II type I receptor, apolipoprotein E (ApoE), endothelial constitutive nitric oxide synthase, and platelet glycoprotein IIIa. Coronary angiography was performed in 94 patients. Coronary angiography showed coronary artery disease in 93% of patients. During follow-up (46 +/- 12 months, range 25 to 72) the overall combined end points (cardiac death, myocardial infarction, and revascularization procedures) accounted for 21 events. Family history of coronary artery disease, smoking, stenosis of the left anterior descending artery at coronary angiography, and ApoE polymorphism (presence of epsilon4 allele) were significantly more prevalent (univariate analysis) in the group of patients with events. Logistic multivariate analysis showed that ApoE polymorphism (P =. 004, odds ratio [OR] 6.8, 95% confidence interval [CI] 2 to 22), family history (P =.005, OR 8.3, 95% CI 2 to 35), smoking after acute myocardial infarction (P =.008, OR 10.9, 95% CI 2 to 62), and left anterior descending coronary artery disease (P =.02. OR 6.6, 95% CI 1.3 to 33) were independent predictors of adverse events. CONCLUSIONS: Myocardial infarction at a young age is commonly characterized by evidence of multiple cardiovascular risk factors and by a favorable prognosis in short- and medium-term follow-up. Evidence of significant disease at coronary angiography suggests the presence of a premature atherosclerotic process. ApoE polymorphism (presence of epsilon4 allele) appears to be a strong independent predictor of adverse events, suggesting a remarkable influence in the accelerated coronary disease.

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.

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.

[Preclinical left ventricular diastolic dysfunction in insulin-dependent diabetes]. / Disfunzione diastolica ventricolare sinistra preclinica nel diabete insulino-dipendente.

BACKGROUND: Isolated alterations of the left ventricular diastolic function have been described in diabetic insulin-dependent patients (IDDM), even in the absence of old age, hypertension, ischemic heart disease, left ventricular hypertrophy. Such alterations have been associated with microangiopathy but it is not known whether it is reversible or if there is a relation with the way the therapy is given. METHODS: Fifty-five subjects have been studied, of which 15 were healthy, 30 recently diagnosed IDDM without microangiopathy and 10 IDDM with microangiopathy. All the patients were under 35 years old and did not present risk factors for coronary artery disease, hypertension or autonomic neuropathy. The maximal exercise stress test proved negative. The diastolic function was studied using the results of Doppler echocardiography of the mitral flow and of isovolumetric relaxation time, with continuous and discrete parameters. RESULTS: The velocity of wave A and E, the relationship between them and their integrals are significantly greater in diabetics with microangiopathy than in those without it and in healthy subjects. There are no significant differences between healthy and diabetic subjects without microangiopathy using continuous parameters. Using discrete parameters diastolic damage is absent in the healthy subjects and is present in 48% of diabetics without microangiopathy and in 90% of those with it. CONCLUSIONS: Slight preclinical diastolic dysfunction is present in young recently diagnosed IDDM without microangiopathy. More severe dysfunction is present when there is also microangiopathy.

[Neural regulation of heart rate. Spectrum analysis of the RR interval in healthy subjects]. / Modulazione neurale della frequenza cardiaca. Analisi spettrale dell'intervallo RR in soggetti sani.

Dynamic 24-hour recordings were obtained in 10 healthy non hospitalized subjects. Spectral analysis of RR interval variabilities provided quantitative markers of sympatho-vagal balance throughout the day and night. The low frequency (0.1 Hz) component was considered a marker of sympathetic activity whereas the high frequency component (0.25 Hz) a marker of vagal tone. We observed an early morning rise in the sympathetic activity markers in all our patients, with a second smaller rise in the early afternoon. We believe this rise may be the trigger of the increased rate of major cardiovascular events reported to happen in the first hours of the morning.

[Propafenone versus hydroquinidine in long-term pharmacological prophylaxis of atrial fibrillation]. / Propafenone versus idrochinidina nella profilassi farmacologica a lungo termine della fibrillazione atriale.

New antiarrhythmic class 1C agents have been proposed in the last few years in an attempt to suppress paroxysmal atrial fibrillation at long-term, as the most commonly used class 1A agents such as quinidine gave highly variable results as regards both side-effects and efficacy. The aim of this randomized prospective study is to evaluate the efficacy and safety of oral propafenone at long term in preventing paroxysmal atrial fibrillation and to compare the results with those obtained using agents such as quinidine. Two hundred patients with recurrent episodes of symptomatic atrial fibrillation were enrolled for this study with entry criteria based upon a history of more than 3 crises in the previous 6 months, with electrocardiographic (standard electrocardiogram or dynamic registration) documentation. According to a randomized selection either propafenone at 300 mg twice daily or hydroquinidine retard 250 mg twice daily were administered to the patients; clinical check-up was carried out every 3 months or if clinical course worsened. The dosages were increased if proved to be inadequate at check-up (i.e. recurrence of atrial fibrillation) up to 300 mg 3 times daily for propafenone and 500 mg twice daily for hydroquinidine. The efficacy at the 3rd month was 71% for propafenone and 60% for hydroquinidine, at the 6th month 60% for propafenone and 56% for hydroquinidine; this trend lowered progressively as the follow-up continued, to 48% for propafenone and 42% for hydroquinidine (NS). More than 70% of the responder patients assumed 600 mg twice for propafenone or 250 twice for hydroquinidine. Propafenone had a percentage of 10% side-effects and hydroquinidine 24% (p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)