The Nobel Prize was created by Alfred Nobel. The first prize was awarded in 1901 and Emil Adolf von Behring was the first laureate in medicine due to his research in diphtheria serum. Regarding cardiology, Nobel Prize’s history permits a global comprehension of progress in pathophysiology, diagnosis and therapeutics of various cardiac diseases in last 120 years. The objective of this study was to review the major scientific discoveries contemplated by Nobel Prizes that contributed to cardiology. In addition, we also hypothesized why Carlos Chagas, one of our most important scientists, did not win the prize in two occasions. We carried out a non-systematic review of Nobel Prize winners, selecting the main studies relevant to heart diseaseamong the laureates. In the period between 1901 and 2013, 204 researches and 104 prizes were awarded in Nobel Prize, of which 16 (15%) studies were important for cardiovascular area. There were 33 (16%) laureates, and two (6%) were women. Fourteen (42%) were American, 15 (45%) Europeans and four (13%) were from other countries. There was only one winner born in Brazil, Peter Medawar, whose career was all in England. Reviewing the history of the Nobel Prize in physiology or medicine area made possible to identify which researchers and studies had contributed to advances in the diagnosis, prevention and treatment of cardiovascular diseases. Most winners were North Americans and Europeans, and male.

BackgroundHeart rate recovery at one minute of rest (HRR1) is a predictor of mortality in heart failure (HF), but its prognosis has not been assessed at six-minute walk test (6MWT) in these patients. ObjectiveThis study aimed to determine the HRR1 at 6MWT in patients with HF and its correlation with six-minute walk distance (6MWD). MethodsCross-sectional, controlled protocol with 161 individuals, 126 patients with stable systolic HF, allocated into 2 groups (G1 and G2) receiving or not β-blocker and 35 volunteers in control group (G3) had HRR1 recorded at the 6MWT. ResultsHRR1 and 6MWD were significantly different in the 3 groups. Mean values of HRR1 and 6MWD were: HRR1 = 12 ± 14 beat/min G1; 18 ± 16 beat/min G2 and 21 ± 13 beat/min G3; 6MWD = 423 ± 102 m G1; 396 ± 101m G2 and 484 ± 96 m G3 (p < 0.05). Results showed a correlation between HRR1 and 6MWD in G1(r = 0.3; p = 0.04) and in G3(r = 0.4; p= 0.03), but not in G2 (r= 0.12; p= 0.48). ConclusionHRR1 response was attenuated in patients using βB and showed correlation with 6MWD, reflecting better exercise tolerance. HRR1 after 6MWT seems to represent an alternative when treadmill tests could not be tolerated.

Background Patients with heart failure (HF) have left ventricular dysfunction and reduced mean arterial pressure (MAP). Increased adrenergic drive causes vasoconstriction and vessel resistance maintaining MAP, while increasing peripheral vascular resistance and conduit vessel stiffness. Increased pulse pressure (PP) reflects a complex interaction of the heart with the arterial and venous systems. Increased PP is an important risk marker in patients with chronic HF (CHF). Non-invasive ventilation (NIV) has been used for acute decompensated HF, to improve congestion and ventilation through both respiratory and hemodynamic effects. However, none of these studies have reported the effect of NIV on PP. ObjectiveThe objective of this study was to determine the acute effects of NIV with CPAP on PP in outpatients with CHF. MethodsFollowing a double-blind, randomized, cross-over, and placebo-controlled protocol, twenty three patients with CHF (17 males; 60 ± 11 years; BMI 29 ± 5 kg/cm2, NYHA class II, III) underwent CPAP via nasal mask for 30 min in a recumbent position. Mask pressure was 6 cmH2O, whereas placebo was fixed at 0-1 cmH2O. PP and other non invasive hemodynamics variables were assessed before, during and after placebo and CPAP mode. ResultsCPAP decreased resting heart rate (Pre: 72 ± 9; vs. Post 5 min: 67 ± 10 bpm; p < 0.01) and MAP (CPAP: 87 ± 11; vs. control 96 ± 11 mmHg; p < 0.05 post 5 min). CPAP decreased PP (CPAP: 47 ± 20 pre to 38 ± 19 mmHg post; vs. control: 42 ± 12 mmHg, pre to 41 ± 18 post p < 0.05 post 5 min). Conclusion NIV with CPAP decreased pulse pressure in patients with stable CHF. Future clinical trials should investigate whether this effect is associated with improved clinical outcome.

Fundamento: A fraqueza muscular inspiratória contribui para a intolerância ao exercício e diminuição da qualidade de vida dos pacientes com insuficiência cardíaca. Estudos com treinamento da musculatura inspiratória demonstram melhora da força muscular inspiratória, da capacidade funcional e da qualidade de vida. Porém, pouco se sabe sobre a resposta hemodinâmica central (RHC) durante o exercício inspiratório (EI). Objetivo: Avaliar a RHC em uma única sessão de EI com diferentes cargas (placebo, 30 e 60%) na insuficiência cardíaca. Métodos: Ensaio clínico randomizado placebo-controlado, em pacientes com insuficiência cardíaca com fração de ejeção reduzida, classe funcional II e III. Vinte pacientes, com idade de 65±11 anos, completaram uma sessão única de exercício inspiratório, em 3 ciclos de 15 minutos, com washout de 1 hora, envolvendo cargas de 30% (C30), 60% (C60) e placebo, utilizando um resistor de carga linear (PowerBreathe Light). O estudo hemodinâmico não invasivo foi realizado por bioimpedância cardiotorácica (Niccomo™CardioScreen®). Análise estatística foi feita com o Teste t de Student e a correlação de Pearson, considerado significante p≤0,05. Resultados: Foi observado aumento da frequência cardíaca (FC) com a C30 (64±15 vs 69±15 bpm; p=0,005) e C60 (67±14 vs 73±14 bpm, p=0,002). No volume sistólico (VS), observou-se diminuição com a C30 (73±26 vs 64±20 ml; p=0,004). O débito cardíaco (DC) apresentou aumento apenas com a C60 (4,6±1,5 vs 5,3±1,7 l/min; p=-0,001). Conclusão: Quando utilizada a carga de 60%, em uma sessão única de EI, foram observadas alterações na RHC. A FC e o DC aumentaram, assim como as escalas de Borg e sensação subjetiva de dispneia. Já a carga de 30% promoveu diminuição do VS.