AimsThe presence of pulmonary hypertension (PH) in left ventricular systolic dysfunction (LVSD) and symptomatic heart failure is an ominous sign. There are insufficient data regarding the risk conferred by increasing severity of PH in patients with heart failure. Methods and resultsWe performed a record linkage study in Tayside, Scotland (population 400 000) utilizing the Tayside echocardiogram database (.50 000 echocardiograms) maintained by the Health Informatics Centre (HIC). Data sets from the HIC include mortality data, cardiovascular medications, and other healthcare activities linked anonymously by the community health index (CHI) number. Patients were included in the analysis if they had LVSD, had a valid right ventricular systolic pressure (RVSP) measurement, and had a loop diuretic prescription (provided not more than 1 year prior to echocardiogram). A Cox proportional hazard model was used to examine the effects of RVSP on all-cause mortality. A total of 1612 patients [mean age, 75.2 + 10.9 (SD) years; 57.4% male] met the entry criteria. Mean RVSP for the cohort was 44.9 + 13.1 mmHg and mean follow-up was 2.8 + 2.5 years. For each 5 mmHg stepwise increase in RVSP, after adjustment for confounding factors including the degree of LVSD and the presence of chronic obstructive pulmonary disease, the hazard ratio (HR) for all-cause mortality was 1.06 (1.03-1.08, P , 0.001). ConclusionsPulmonary hypertension predicted all-cause mortality in a heterogeneous group of patients with heart failure. Each 5 mmHg rise in RVSP was associated with a 6% increased risk of death.--

Heart failure (HF) is a very common condition that, despite advances in treatment, carries significant morbidity and mortality. Although there is good evidence for the treatment of HF with reduced ejection fraction (HFrEF), the treatment for HF with preserved ejection fraction (HFpEF) is not well defined. The renin-angiotensin-aldosterone system (RAAS) has been shown to be an effective target in the treatment of HFrEF using angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone blockade, although the evidence in HFpEF is less clear. This review aims to look first at the evidence for these drugs, and second at the newer drugs that act on the RAAS, namely, direct renin inhibitors, neutral endopeptidase inhibitors, vasopeptidase inhibitors, and angiotensin receptor blockers.

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Objective To examine the relationship between the mean of all HbA1c measures after CHF diagnosis and outcome in a large cohort of T2DM patients with incident CHF. Design Retrospective, observational cohort study. Setting Tayside, Scotland. Patients T2DM patients with incident CHF between 1993 and 2010. Measurement A weighted mean HbA1c was calculated using all available HbA1c measures following CHF diagnosis and patients were grouped into five categories of HbA1c (#6%, >6e#7%, >7e#8%, >8e#9% and >9%). We subsequently compared diet and drug treated populations. The relationship between mean HbA1c and all-cause deaths after CHF diagnosis was assessed. Results 795 patients with T2DM met study criteria. Median followup of 3.8 years saw 491 (61.8%) deaths. Cox regression model, adjusted for all other significant predictors, with the middle HbA1c category (>7e#8%) as the reference, showed a U shaped relationship between HbA1c and outcome. (<6% [HR 95% CI 1.78 (1.26 to 2.52)]; >6e#7% [1.29 (1.01 to 1.66)] and >9% [1.38 (1.03 to 1.84)]. We found a similar relationship in the drug treated subgroup. However in the diet only group, low HbA1c was associated with the lowest risk of death (#7% [0.17 (0.07 to 0.39)]). Conclusions In patients with T2DM and CHF, our observational study shows that in drug treated patients there was a U shaped relationship between HbA1c and mortality with the lowest mortality risk in patients with modest glycaemic control (HbA1c, >7e#9%). However in diet treated patients, lower HbA1c was associated with lower mortality risk.

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