Deficiência de ferro na insuficiência cardíaca: [revisão] / Iron deficiency in heart failure patients: [review]

A anemia é uma comorbidade frequente nos pacientes com insuficiência cardíaca (IC) e sua presença parece estar associada à pior evolução, sendo descrita em alguns estudos como fator de prognóstico independente tanto na IC sistólica quanto na diastólica. Entretanto, ainda não sabemos se a anemia causa pior evolução ou se é apenas um marcador do maior comprometimento cardíaco nos portadores de IC. A etiologia da anemia na IC é multifatorial e parece variar conforme a população estudada. Os fatores como a deficiência nutricional de ferro, presença de insuficiência renal, intensa atividade inflamatória sistêmica, uso de medicações que inibem a produção de eritropoetina ou que causam perda sanguínea são os mais frequentes causadores de anemia na IC. A prevalência de anemia citada nos estudos de IC é muito variável (de 9 por cento a 79,1 por cento) e isto é dependente da população estudada, da fase da cardiopatia, do método e referências hematimétricas utilizadas para diagnóstico. A deficiência de ferro é um importante fator etiológico e está presente em um número significativo de pacientes com anemia e IC associada. Em estudo realizado em nosso grupo, a incidência de deficiência de ferro nos pacientes com anemia foi de 61,8 por cento. Portanto, a anemia é um achado frequente, sua presença acentua as manifestações clínicas da IC e está associada a piora do prognóstico. Conhecer a causa da anemia facilita o seu tratamento e, apesar da sua correção ainda não ser consenso, os pacientes sem anemia têm melhor evolução.

Anemia is common in heart failure (HF) patients with its presence apparently associated to a worse prognosis, and as such is described in some studies as an independent predictor of death and hospitalization of patients suffering from systolic and diastolic dysfunction. It remains unknown whether anemia causes the worse evolution of HF patients or whether it is only one marker of a worse heart disease stage. The etiology of anemia is multifactorial and seems to change dependent on the studied population. Factors such as nutritional iron deficiency, presence of kidney failure, intense systematic inflammatory activity, medication use that inhibits the production of erythropoietin or that results in blood loss are the most frequent causes of anemia in heart disease. The prevalence of anemia reported in studies of HF is very variable (from 9 to 79.1 percent) and is dependent of the studied population, stage of heart disease and method and references used for diagnosis. Iron deficiency is an important etiologic factor which is present in a significant number of patients with the association of anemia and HF. In a study carried out by our group, the incidence of iron deficiency in anemic patients was 61.8 percent. Hence, anemia is a frequent finding; its presence accentuates the clinical manifestations of HF and is associated to a worse prognosis. An understanding of the cause of anemia makes treatment easier and although there is no consensus on its correction, patients without anemia have a better evolution.

Sympathetic nerve activity restrains reflex vasodilatation in heart failure.

BACKGROUND: Blunted reflex muscle vasodilatory response during exercise in heart failure (HF) patients may be secondary to augmented vasoconstriction. We tested the hypothesis that the exaggerated sympathetic nerve activity restrains the reflex muscle vasodilatation during exercise in HF patients. METHODS: We studied the reflex vasodilatory response (plethysmography) during 3 min static handgrip exercise at 30% maximal voluntary contraction in 10 advanced HF patients (45 +/- 3 year, NYHA Functional Class III/IV) and 10 age-matched normal controls (NC, 40 +/- 3 year, P = 0.23) during intra-arterial infusion of: (1) saline control; and (2) alpha-adrenergic blocker (phentolamine). RESULTS: Baseline forearm vascular conductance (FVC) was lower in HF patients than in NC (2.07 +/- 0.2 vs. 4.26 +/- 0.6 units, respectively; P = 0.002). FVC responses during exercise increased significantly in NC, but not in HF patients (delta changes: 1.05 +/- 0.4 vs. 0.05 +/- 0.2 units, respectively). Phentolamine significantly increased resting FVC in HF patients (from 2.07 +/- 0.2 to 5.74 +/- 0.7 units, P = 0.00004) and restored reflex vasodilatory responses during exercise (delta changes: from 0.05 +/- 0.2 to 1.82 +/- 0.9 units) eliminating the difference in FVC between both groups. CONCLUSIONS: The blunted reflex muscle vasodilatory response during exercise in advanced HF patients is, at least in part, due to the increase in sympathetic nerve activity.

The effects of exercise training on sympathetic neural activation in advanced heart failure: a randomized controlled trial.

OBJECTIVES: The goal of this study was to test the hypothesis that exercise training reduces resting sympathetic neural activation in patients with chronic advanced heart failure. BACKGROUND: Exercise training in heart failure has been shown to be beneficial, but its mechanisms of benefit remain unknown. METHODS: Sixteen New York Heart Association class II to III heart failure patients, age 35 to 60 years, ejection fraction < or =40% were divided into two groups: 1) exercise-trained (n = 7), and 2) sedentary control (n = 9). A normal control exercise-trained group was also studied (n = 8). The four-month supervised exercise training program consisted of three 60 min exercise sessions per week, at heart rate levels that corresponded up to 10% below the respiratory compensation point. Muscle sympathetic nerve activity (MSNA) was recorded directly from peroneal nerve using the technique of microneurography. Forearm blood flow was measured by venous plethysmography. RESULTS: Baseline MSNA was greater in heart failure patients compared with normal controls; MSNA was uniformly decreased after exercise training in heart failure patients (60 +/- 3 vs. 38 +/- 3 bursts/100 heart beats), and the mean difference in the change was significantly (p < 0.05) greater than the mean difference in the change in sedentary heart failure or trained normal controls. In fact, resting MSNA in trained heart failure patients was no longer significantly greater than in trained normal controls. In heart failure patients, peak VO(2) and forearm blood flow, but not left ventricular ejection fraction, increased after training. CONCLUSIONS: These findings demonstrate that exercise training in heart failure patients results in dramatic reductions in directly recorded resting sympathetic nerve activity. In fact, MSNA was no longer greater than in trained, healthy controls.

Weight loss improves neurovascular and muscle metaboreflex control in obesity.

We studied the effects of a hypocaloric diet (D, n = 24, age: 32.2 +/- 1.4 yr, body mass index: 34.7 +/- 0.5 kg/m2) and a hypocaloric diet associated with exercise training (D + T, n = 25, age: 32.3 +/- 1.3 yr, body mass index: 32.9 +/- 0.4 kg/m2) on muscle metaboreflex control, muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, and forearm blood flow (plethysmography) levels during handgrip exercise at 10% and 30% of maximal voluntary contraction in normotensive obese women. An additional 10 women matched by age and body mass index were studied as a nonadherent group. D or D + T significantly decreased body mass index. D or D + T significantly decreased resting MSNA (bursts/100 heartbeats). The absolute levels of MSNA were significantly lower throughout 10% and 30% exercise after D or D + T, although no change was found in the magnitude of response of MSNA. D + T, but not D, significantly increased resting forearm vascular conductance. D + T significantly increased the magnitude of the response of forearm vascular conductance during 30% exercise. D or D + T significantly increased MSNA levels during posthandgrip circulatory arrest when muscle metaboreflex is isolated. In conclusion, weight loss improves muscle metaboreflex control in obese women. Weight loss reduces MSNA, which seems to be centrally mediated. Weight loss by D + T increases forearm vascular conductance at rest and during exercise in obese individuals.

Postexercise blood pressure reduction in elderly hypertensive patients.

OBJECTIVES: We sought to study: 1) the impact of hemodynamic and left ventricular function on short-term postexercise blood pressure reduction in elderly hypertensive patients; and 2) the 22-h postexercise effects on ambulatory blood pressure in elderly hypertensive patients. BACKGROUND: Although early exercise provokes postexercise blood pressure reduction, the mechanisms underlying this response are not completely understood. Besides, it is unclear whether the reduction in blood pressure after exercise lasts long enough to have clinical relevance in elderly hypertensive patients. METHODS: We studied 24 elderly hypertensive patients (age 68.9 +/- 1.5 years) and 18 age-matched normotensive control subjects (age 68.1 +/- 1.2 years). Cardiac output (carbon dioxide rebreathing) and blood pressure (auscultatory) were measured at rest and after a 45-min period of low-intensity bicycle exercise (50% maximal oxygen uptake) and at 15, 30, 60 and 90 min after exercise. Left ventricular function (by Doppler echocardiography) was also evaluated. Ambulatory blood pressure monitoring was evaluated after 45 min of exercise or 45 min of rest, in a randomized order. RESULTS: In the hypertensive patients, exercise provoked a significant reduction in blood pressure, cardiac output, stroke volume and left ventricular end-diastolic volume. It also provoked a significant reduction in systolic, mean and diastolic blood pressure during a 22-h period, at daytime and nighttime. CONCLUSIONS: The short-term reduction in blood pressure after exercise in elderly hypertensive patients is associated with a decrease in stroke volume and left ventricular end-diastolic volume. The 22-h postexercise reduction in blood pressure demonstrates the clinical relevance of low-intensity exercise in elderly hypertensive patients.

Cardiomiopatia hipertrófica em gerontos: dados clínicos e evolutivos / Hipertrophic cardiomyopathy in the elderly: clinical and evolutive data

Neste trabalho foram estudados 19 pacientes portadores de cardiomiopatia hipertrófica com idade média de 69 anos (12 homens e 7 mulheres), 17 dos quais (95%) com forma obstrutiva. Todos foram submetidos à avaliaçäo clínica, eletro e ecodopplercardiográfica. Eletrocardiografia contínua foi realizada em 16 casos e estudo hemodinâmico e angiocardiográfico em 9. Dos 18 pacientes vivos, 9 estäo recebendo bloqueadores beta - adrenérgticos, 8 bloqueadores dos canais de cálcio e 5 amiodarona. O seguimento médio foi de 98 meses. Quatorze pacientes (73%) estäo em classe funcional (CF) I e 4 (21%) em CFII. Ocorreu apenas um óbito (5%). O eletrocardiograma estava alterado em todos os pacientes, tendo sido observada SVE em 94%, índice acima do descrito na literatura. Ao estudo ecodopplercardiográfico observamos calcificaçäo do anel mitral em 26% dos pacientes, abaixo do referido na literatura. Espessamento dos folhetos da valva aórtica foi encontrado em 31% dos casos, o que näo tem sido descrito. Arritmia supra-ventricular foi observada em 87% e ventricular em 100%, sendo taquicardia ventricular näo-sustentada (TVNS) em 31%, acima da média da literatura. Concluímos que cardiomiopatia hipertrófica em gerontes näo é infreqüente e que seu diagnóstico, hoje em dia, é facilitado pela ecodopplercardiografia. A elevada incidência de arritmias complexas näo parece ter relaçäo com a morte súbita