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In an acute, double-blind, crossover study on 12 patients with essential hypertension, the interaction between nifedipine and prazosin was investigated in the supine position. The effectiveness of the combination of the two active drugs was greater than the combination of either of the drugs plus placebo. The effect of nifedipine was not modified by prazosin pretreatment; however, the effect of prazosin was partly inhibited, i.e., delayed, by nifedipine pretreatment. Therefore, giving prazosin as a first drug and nifedipine as the second drug seems to be a better approach than the reverse.

Clinical and experimental evidence for important interactions between platelets and vascular endothelium under conditions of myocardial ischemia is briefly summarized. The clinical evidence for a role of platelets in myocardial ischemia includes studies indicating alterations in platelet behavior and the therapeutic benefit of some antiplatelet drugs. Experimental evidence suggesting the importance of platelets in ischemia includes reductions in transmyocardial platelet number under these conditions, the cyclical reductions in coronary blood flow that result from intermittent intravascular platelet aggregation, and the relationship between induced platelet aggregation and cardiac arrhythmias. Evidence strongly suggesting the importance of platelet emboli and thromboxane generation as a major cause of reperfusion-induced ventricular arrhythmias is outlined.

Myocardial galectin-3 is upregulated upon cardiac stressors such as angiotensin II and pressure overload leading to cardiac remodeling and heart failure. The expression level of galectin-3 mirrors the progression and severity of heart failure and therefore, galectin-3 is being used as a biomarker for heart failure. However, as galectin-3 is causally involved in pathological myocardial fibrosis it has been suggested that galectin-3 also actively contributes to heart failure development. In this review we discuss how galectin-3 could be a target for therapy in heart failure. Currently, attempts are being made to target or inhibit galectin-3 using natural or pharmaceutical inhibitors with the aim to ameliorate heart failure. Available experimental evidence suggests that galectin-3 inhibition indeed may represent a novel tool to treat heart failure. A strong interaction with aldosterone, another strong pro-fibrotic factor, has been described. Clinical studies are needed to prove if galectin-3 may be used to install specific treatment regimens.

Môi trường vi mô cơ học tại chỗ ảnh hưởng đến hành vi của tế bào. Trong hệ tim mạch, các tế bào trong cả tim và mạch máu đều chịu tác động của dòng máu liên tục, áp lực máu, lực kéo căng và độ cứng thay đổi của ma trận ngoại bào. Các tín hiệu do lực gây ra sẽ di chuyển tới nhân tế bào, điều chỉnh các thay đổi về di truyền học như động học chromatin và biểu hiện gen. Các dấu hiệu cơ học là cần thiết ở giai đoạn rất sớm để phát triển phôi thai chính xác, trong khi ở giai đoạn sau của đời sống, các tín hiệu cơ học bất thường có thể dẫn đến một loạt các bệnh lý, bao gồm nhiều loại bệnh tim mạch khác nhau. Do đó, một nghiên cứu về sự biến đổi di truyền học do lực sinh ra ở các khoảng thời gian khác nhau là cần thiết để hiểu đầy đủ các thay đổi về hình thái trong sự khởi đầu và tiến triển của bệnh. Vì lý do đó, cơ học di truyền học tim mạch nổi lên như một lĩnh vực nghiên cứu hấp dẫn. Với những tiến bộ nhanh chóng trong lĩnh vực nghiên cứu mới mẻ này, bài tổng quan ngắn này nhằm cung cấp phân tích về trạng thái kiến thức hiện có về các thay đổi di truyền học do lực gây ra trong lĩnh vực tim mạch.

In blacks and whites of similar socioeconomic background, the incidence of pregnancy-induced hypertension (PIH) is probably the same. In underdeveloped coutries, however, PIH is often a life-threatening complication of pregnancy. Recent theories as to the etiology of PIH include the suggestion that vascular tone may be increased as a result of inhibition of active sodium transport in vascular smooth muscle. This may be the result of an inhibitor of sodium transport present in the serum. The literature concerning the demonstration of endogenous sodium transport inhibitors and endogenous digoxinlike immunoreactivity (EDLI) in PIH is reviewed and discussed.

To assess the clinical effects and safety profile of initial monotherapy with either bisoprolol or enalapril in elderly patients with heart failure (HF). In CIBIS III, 1010 patients with mild to moderate HF and age ≥65 years were randomized to monotherapy with either bisoprolol or enalapril for 6 months. Bisoprolol had a similar effect as enalapril on the combined end-point of all-cause mortality or hospitalization (HR 1.02; p = 0.90), as well as on each of the individual end-points. A trend towards fewer sudden deaths was observed with bisoprolol (NS). On the other hand, more cases of worsening HF requiring hospitalization or occurring while in hospital were observed in the bisoprolol group (HR 1.67; p = 0.03). The two groups were similar with regard to treatment cessations and early introduction of the second drug. Bisoprolol and enalapril had a similar effect on the combined end-point of mortality or hospitalization during 6 months monotherapy. However, more worsening HF events were observed in the bisoprolol group.

Thrombolytic trials in acute myocardial infarction have progressively increased in size, with the GUSTO study including over 40,000 patients. New thrombolytic drugs are unlikely to lead to further major reductions in fatality, and demonstrating small differences from existing compounds would require even larger trials to establish mortality benefits. New agents may, however, have advantages, such as a greater ease of administration or a reduced cost, and the problem is how to assess such new agents in the most efficient way. The concept of equivalence as a clinical trial endpoint is discussed, and the INJECT study, comparing reteplase and streptokinase in acute myocardial infarction, is described as a prototype equivalence trial.

Atrial fibrillation (AF) is the most common arrhythmia and has an increasing impact on public health because of its morbidity and mortality. Clinical and diagnostic tests to predict the recurrence of arrhythmia and clinical events before AF becomes permanent are still an open issue. 307 out of 1442 patients in sinus rhythm, at high risk of recurrence of AF enrolled in the GISSI-AF study, participated in a substudy with echocardiographic and biohumoral evaluation at baseline and at 12-month follow-up. The relations between biomarker concentrations and echocardiographic parameters with study endpoints in 1 year, were analysed by a stepwise multivariable Cox model (entry criteria p < 0.5 and stay criteria p < 0.2). The echocardiographic variables, cardiac markers and clinical variables considered in the statistical model indicated a higher concentration of NT-proBNP at baseline as the strongest factor related to time of first AF recurrence (HR 1.42; 95 %CI 1.23–1.46), first CV hospitalization (HR 1.58; 95 %CI 1.31–1.92) and increasing duration of recurrent AF (OR 2.16; 95 %CI 1.52–3.08). Valsartan treatment was not related to clinical events. In patients in sinus rhythm with a history of AF a higher concentration of NT-proBNP at baseline was the strongest independent risk factor for first AF recurrence and its duration, and for the first hospital admission for cardiovascular reasons.