Background Heart failure (HF) and non-cardiac comorbidities often coexist and are known to have an adverse effect on outcome. However, the prevalence and prognostic impact of non-cardiac comorbidities in patients with HF with reduced ejection fraction (HFrEF) vs. those with preserved (HFpEF) remain inadequately studied. Methods and results We used data from the Swedish Heart Failure Registry from 2000 to 2012. HFrEF was defined as EF < 50% and HFpEF as EF ≥ 50%. Of 31 344 patients available for analysis, 79.3% ( n = 24 856) had HFrEF and 20.7% ( n = 6 488) HFpEF. The outcome was all-cause mortality. We examined the association between ten non-cardiac comorbidities and mortality and its interaction with EF using adjusted hazard ratio (HR). Stroke, anemia, gout and cancer had a similar impact on mortality in both phenotypes, whereas diabetes (HR 1.57, 95% confidence interval [CI] [1.50–1.65] vs. HR 1.39 95% CI [1.27–1.51], p = 0.0002), renal failure (HR 1.65, 95% CI [1.57–1.73] vs. HR 1.44, 95% CI [1.32–1.57], p = 0.003) and liver disease (HR 2.13, 95% CI [1.83–2.47] vs. HR 1.42, 95% CI [1.09–1.85] p = 0.02) had a higher impact in the HFrEF patients. Moreover, pulmonary disease (HR 1.46, 95% CI [1.40–1.53] vs. HR 1.66 95% CI [1.54–1.80], p = 0.007) was more prominent in the HFpEF patients. Sleep apnea was not associated with worse prognosis in either group. No significant variation was found in the impact over the 12-year study period. Conclusions Non-cardiac comorbidities contribute significantly but differently to mortality, both in HFrEF and HFpEF. No significant variation was found in the impact over the 12-year study period. These results emphasize the importance of including the management of comorbidities as a part of a standardized heart failure care in both HF phenotypes.

BackgroundA number of registry studies have reported suboptimal adherence to guidelines for cardiovascular prevention during the first year after acute myocardial infarction (AMI). However, only a few studies have addressed long-term secondary prevention after AMI. This study evaluates prevention guideline adherence and outcome of guideline-directed secondary prevention in patients surviving 2 years after AMI.MethodsPatients aged 18–85 years at the time of their index AMI were consecutively identified from hospital discharge records between July 2010 and December 2011 in Gothenburg, Sweden. All patients who agreed to participate in the study (16.2%) were invited for a structured interview, physical examinations and laboratory analysis 2 years after AMI. Guideline-directed secondary preventive goals were defined as optimally controlled blood pressure, serum cholesterol, glucose, regular physical activity, smoking cessation and pharmacological treatment.ResultsThe mean age of the study cohort (n = 200) at the index AMI was 63.0 ± 9.7 years, 79% were men. Only 3.5% of the cohort achieved all six guideline-directed secondary preventive goals 2 years after infarction. LDL < 1.8 mmol/L was achieved in 18.5% of the cohort, regular exercise in 45.5% and systolic blood pressure <140 mmHg in 57.0%. Anti-platelet therapy was used by 97% of the patients, beta-blockers by 83.0%, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers by 76.5% and statins by 88.5%. During follow-up, non-fatal adverse cardiovascular events (cardiac hospitalization, recurrent acute coronary syndrome, angina pectoris, new percutaneous coronary intervention, new onset of atrial fibrillation, post-infarct heart failure, pacemaker implantation, stroke/transient ischemic attack (TIA), cardiac surgery and cardiac arrest) occurred in 47% of the cohort and readmission due to cardiac causes in 30%.ConclusionsOur data showed the failure of secondary prevention in our daily clinical practice and high rate of non-fatal adverse cardiovascular events 2 years after AMI.

BackgroundResting heart rate (RHR), a known cardiovascular risk factor, changes with age. However, little is known about the association between changes in RHR and the risk of cardiovascular events. The purpose of this study was therefore to assess the impact of RHR at baseline, and the change in RHR over time, on the risk of all-cause death and cardiovascular events.DesignA random population sample of men born in 1943 who were living in Gothenburg, Sweden was prospectively followed for a 21-year period.MethodsParticipants were examined three times: first in 1993 and then re-examined in 2003 and 2014. At each visit, a clinical examination, an ECG and laboratory analyses were performed. Change in RHR between 1993 and 2003 was defined as a decrease if RHR decreased by 5 beats per minute (bpm), an increase if RHR increased by 5 bpm or stable if the RHR change was <4bpm).ResultsParticipants with a baseline RHR of >75 bpm in 1993 had about a twofold higher risk of all-cause death (HR 2.3, CI 1.2 to 4.7, p=0.018), cardiovascular disease (CVD) (HR 1.8, CI 1.1 to 3.0, p=0.014) and coronary heart disease (CHD) (HR 2.2, CI 1.1 to 4.5, p=0.025) compared with those with <55 bpm in 1993. Participants with a stable RHR between 1993 and 2003 had a 44% decreased risk of CVD (HR 0.56, CI 0.35 to 0.87, p=0.011) compared with participants with an increasing RHR. Furthermore, every beat increase in heart rate from 1993 was associated with a 3% higher risk for all-cause death, 1% higher risk for CVD and 2% higher risk for CHD.ConclusionHigh RHR was associated with an increased risk of death and cardiovascular events in men from the general population. Moreover, individuals with an increase in RHR between 50 and 60 years of age had worse outcome.

BackgroundDespite a decline in mortality rates from cardiovascular disease (CVD) in the past few decades, the burden of CVD in a contemporary population remains inadequately addressed. Therefore, this study was aimed to investigate secular trends in mortality from coronary artery disease and all‐cause mortality over 2 decades, by comparing 2 cohorts of men born 30 years apart and evaluate the prediction of the risk of CVD and all‐cause death in a contemporary random sample of Swedish men.Methods and ResultsTwo cohorts of randomly selected men born in 1913 (855 men) and 1943 (798 men) were first examined at age 50 in 1963 and 1993, respectively, and followed longitudinally over 21 years. All‐cause mortality and coronary artery disease death were lower in 50‐ to 71‐year‐old men born in 1943 compared with those born in 1913, with unadjusted hazard ratios of 0.57 (0.45–0.71) and 0.34 (0.22–0.53), respectively. After adjustment for risk factors (smoking, serum cholesterol, hypertension, systolic blood pressure, diabetes mellitus, body mass index, and physical activity), the differences between the cohorts remained significant for coronary artery disease, hazard ratios 0.57 (0.34–0.94), P=0.029, but not for all‐cause mortality hazard ratios 0.82 (0.62–1.07), P=0.14. However, the rate of CVD events during follow‐up was still high (30.7%) for the men born in 1943. No statistically significant interaction by birth cohort in contribution of risk factors to death was found between 2 cohorts except physical inactivity.ConclusionsDespite a marked reduction in the rate of coronary artery disease death over the past 30 years, the burden of CVD events and all‐cause mortality remains high. Therefore, intensified efforts to modify contributing risk factors are still required.

Left atrial enlargement has been shown to be associated with obstructive sleep apnea in patients with coronary artery disease and in sleep clinic cohorts. However, data from the general population are limited. The aim of this study was to investigate whether there is an association between obstructive sleep apnea and left atrial enlargement in a random sample from a general population of 71-year-old men. As part of the longitudinal population study The Study of Men Born in 1943, we analysed cross-sectional data for 411 men, all 71 years old, who had participated in an overnight home sleep study and a standardized echocardiographic examination. Of the 411 men, 29.4% had moderate to severe obstructive sleep apnea [apnea-hypopnea index score of ≥15 (n = 121)]. These participants showed a significantly higher frequency of systolic heart failure, hypertension, overweight, had greater waist circumference as well as higher left atrial areas compared with men with no or mild obstructive sleep apnea (23.7 ± 5.5 cm versus 21.6 ± 4.5 cm , P < 0.001). In a linear regression analysis, obstructive sleep apnea was significantly associated with left atrial enlargement after adjusting for overweight, atrial fibrillation, heart failure with reduced ejection fraction, hypertension and mitral regurgitation. Compared with individuals without obstructive sleep apnea, the mean left atrial area was 1.7 ± 1.5 cm larger in men with severe obstructive sleep apnea (P < 0.05) and 1.3 ± 1.1 cm larger among men with moderate obstructive sleep apnea (P < 0.05). In this cross-sectional study of 71-year-old men from the general population, left atrial area was independently associated with prevalence and severity of obstructive sleep apnea.

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Background Knowledge about long-term risk factors and the prevalence of heart failure stages in general population is limited. We aimed to study the prevalence of cardiac dysfunction and heart failure in 71-year-old men and potential risk factors in the past two decades. Design This research was based on a randomized selected population study with longitudinal follow-up. Methods A random sample of men born in 1943 in Gothenburg, Sweden were examined in 1993 (at 50 years of age) and re-examined 21 years later in 2014 (at 71 years of age). Cardiac dysfunction or heart failure was classified into four stages (A–D) according to American Heart Association/American College of Cardiology guidelines on heart failure. Results Of the 798 men examined in 1993 (overall cohort), 535 (67%) were re-examined in 2014 (echo cohort). In the echo cohort 122 (23%) men had normal cardiac function, 135 (25%) were at stage A, 207 (39%) men were at stage B, 66 (12%) men were at stage C, and five (1%) men were at stage D. Multivariable logistic regression demonstrated that elevated body mass index at 50 years old was the only independent risk factor for developing heart failure/cardiac dysfunction during the subsequent 21 years. For each unit (1 kg/m2) of increased body mass index, the odds ratio for stages C/D heart failure vs no heart failure/stage A increased by 1.20 (95% confidence interval, 1.11–1.31, p < 0.001), after adjustment for smoking, sedentary life style, systolic blood pressure, diabetes, and hyperlipidemia. Conclusion In a random sample of men at 71 years of age, half presented with either cardiac dysfunction or clinical heart failure. High body mass index was associated with an increased risk for developing cardiac dysfunction or heart failure over a 21-year period.