Effect of Cardiorespiratory Fitness on Co-Morbidities and Mortality in Never, Past, and Current Smokers.

Smoking is a strong risk factor for cardiovascular (CV) disease and mortality, but quitting may cause weight gain and increase the risk of co-morbidities. Our aim was to investigate the effect of smoking and exercise on weight-associated co-morbidities and mortality. We included Minnesota residents without baseline CV disease who underwent exercise testing from 1993 to 2010. Mortality was determined from Mayo Clinic records and Minnesota Death Index. Total, CV and cancer mortality by smoking status and cardiorespiratory fitness (CRF): (1) <80%, (2) 80% to 99%, (3) ≥100%. Differences were tested using logistic and Cox regression adjusting for age and gender. A total of 21,981 patients (7,090 past, 2,464 current smokers) were included. Past smokers had more obesity, hypertension, diabetes, and low CRF compared with never smokers. Current smokers did not show increased risk factor prevalence compared with never smokers but had higher rates of low CRF. There were 1,749 deaths; mean follow-up was 12 ± 5 years. Mortality was only slightly increased in past versus never smokers (Hazard Ratio: 1.2; 95% confidence interval 1.12 to 1.38) but was much higher in current smokers (Hazard Ratio 2.4; 95% confidence interval 2.05 to 2.80). Mortality in never, past, and current smokers was inversely related to CRF level. In conclusion, past smokers showed higher rates of co-morbidities and low CRF, but mortality was only mildly increased versus never smokers, whereas current smokers carried a high mortality risk. Our data suggest that quitting smoking is beneficial despite the increased co-morbidities. Exercise may potentially mitigate the risk of co-morbidities and death in those who quit smoking.

Significance of an Increase in Diastolic Blood Pressure During a Stress Test in Terms of Comorbidities and Long-Term Total and CV Mortality.

BACKGROUND: A decrease in diastolic blood pressure (DBP) with exercise is considered normal, but the significance of an increase in DBP has not been validated. Our aim was to determine the relationship of DBP increasing on a stress test regarding comorbidities and mortality. METHODS: Our database was reviewed from 1993 to 2010 using the first stress test of a patient. Non-Minnesota residence, baseline cardiovascular (CV) disease, rest DBP <60 or >100 mm Hg, and age <30 or ≥80 were exclusion criteria. DBP response was classified: normal if peak DBP-rest DBP < 0, borderline 0-9, and abnormal ≥10 mm Hg. Mortality was determined from Mayo Clinic records and Minnesota Death Index. Logistic regression was used to determine the relationship of DBP response to the presence of comorbidities. Cox regression was used to determine total and CV mortality risk by DBP response. All analyses were adjusted for age, sex, and resting DBP. RESULTS: Twenty thousand seven hundred sixty patients were included (51 ± 11 years, female n = 7,314). Rest/peak averaged DBP 82 ± 8/69 ± 15 mm Hg in normal vs. 79 ± 9/82 ± 9 mm Hg in borderline vs. 76 ± 9/92 ± 11 mm Hg in abnormal DBP response. There were 1,582 deaths (8%) with 557 (3%) CV deaths over 12 ± 5 years of follow-up. In patients with borderline and abnormal DBP response, odds ratios for obesity, hypertension, diabetes, and current smoking were significant, while hazard ratios for total and CV death were not significant compared with patients with normal DBP response. CONCLUSIONS: DBP response to exercise is significantly associated with important comorbidities at the time of the stress test but does not add to the prognostic yield of stress test.

Prognostic Performance of Heart Rate Recovery on an Exercise Test in a Primary Prevention Population.

BACKGROUND: Heart rate (HR) recovery has been investigated in specific patient cohorts, but there is less information about the role of HR recovery in general populations. We investigated whether HR recovery has long-term prognostic significance in primary prevention. METHODS AND RESULTS: Exercise tests performed between 1993 and 2010 on patients aged 30 to 79 years without cardiovascular disease were included. Mortality was determined from Mayo Clinic records and Minnesota Death Index. Total, cardiovascular, and non-cardiovascular mortality was reported according to HR recovery <13 bpm using Cox regression. 19 551 patients were included, 6756 women (35%), age 51±10 years. There were 1271 deaths over follow-up of 12±5 years. HR recovery declined after age 60, and was also lower according to diabetes mellitus, hypertension, obesity, current smoking, and poor cardiorespiratory fitness but not sex or ß-blockers. Adjusting for these factors, abnormal HR recovery was a significant predictor of total (hazard ratio [95% confidence interval]=1.56 [1.384-1.77]), cardiovascular (1.95 [1.57-2.42]), and non-cardiovascular death (1.41 [1.22-1.64]). Hazard ratios for cardiovascular death according to abnormal HR recovery were significant in all age groups (30-59, 60-69, 70-79), in both sexes, in patients with and without hypertension, obesity, and diabetes mellitus, but not in patients taking ß-blockers, current smokers, and patients with normal cardiorespiratory fitness. CONCLUSIONS: HR recovery is a powerful prognostic factor predicting total, cardiovascular, and non-cardiovascular death in a primary prevention cohort. It performs consistently well according to sex, age, obesity, hypertension, and diabetes mellitus but shows diminished utility in patients taking ß-blockers, current smokers, and patients with normal cardiorespiratory fitness.

Detailed heart rate variability analysis in athletes.

OBJECTIVE: Heart rate variability (HRV) analysis has been used to evaluate patients with various cardiovascular diseases. While the vast majority of HRV studies have focused on pathological states, our study focuses on the less explored area of HRV analysis across different training intensity and sports. We aimed to measure HRV in healthy elite and masters athletes and compare to healthy, but non-athletic controls. METHODS: Time-domain HRV analysis was applied in 138 athletes (male 110, age 28.4 ± 8.3) and 100 controls (male 56, age 28.3 ± 6.9) during Holter monitoring (21.3 ± 3.0 h). RESULTS: All studied parameters were higher in elite athletes compared to controls [SDNN (CI) 225.3 (216.2-234.5) vs 158.6 (150.2-167.1) ms; SDNN Index (CI) 99.6 (95.6-103.7) vs 72.4 (68.7-76.2) ms; pNN50 (CI) 24.2 (22.2-26.3) vs 14.4 (12.7-16.3) %; RMSSD (CI) 71.8 (67.6-76.2) vs 50.8 (46.9-54.8) ms; p < 0.001]. Masters had higher HRV values than controls, but no significant differences were found between elite athletes and masters athletes. Some parameters were higher in canoeists-kayakers and bicyclists than runners. Lower cut-off values in elite athletes were SDNN: 147.4 ms, SDNN Index: 66.6 ms, pNN50: 9.7 %, RMSSD: 37.9 ms. INTERPRETATION: Autonomic regulation in elite athletes described with HRV is significantly different than in healthy controls. Sports modality and level of performance, but not age- or sex-influenced HRV. Our study provides athletic normal HRV values. Further investigations are needed to determine its role in risk stratification, optimization of training, or identifying overtraining.

Impaired Heart Rate Response to Exercise in Diabetes and Its Long-term Significance.

OBJECTIVE: To investigate the effect of diabetes mellitus on exercise heart rate and the role of impaired heart rate in excess mortality in diabetes. PATIENTS AND METHODS: Patients without cardiovascular disease who underwent exercise testing from September 1, 1993, through December 31, 2010, were included. Mortality was determined from Mayo Clinic records and the Minnesota Death Index. Multivariate linear regression was used to compare heart rate responses in patients with vs without diabetes. Cox regression was used to determine the effect of abnormal heart rate recovery and abnormal chronotropic index on survival. RESULTS: A total of 21,396 patients (65.4% men) with a mean ± SD age of 51±11 years, including 1200 patients with diabetes (5.4%), were included. Patients with diabetes had a higher resting heart rate (81±14 vs 77±13 beats/min), lower peak heart rate (154±20 vs 165±19 beats/min), heart rate reserve (73±19 vs 88±19 beats/min), chronotropic index (0.86±0.22 vs 0.99±0.20), and heart rate recovery (15±8 vs 19±9 beats/min) vs patients without diabetes. There were 1362 deaths (6.4%) during a mean ± SD follow-up of 11.9±4.9 years. Adjusting for age, sex, and heart rate-lowering drug use, a chronotropic index less than 0.8 contributed significantly to risk in patients with diabetes (hazard ratio [HR], 2.21; 95% CI, 1.62-3.00; P<.001) and patients without diabetes (HR, 1.94; 95% CI, 1.71-2.20; P<.001), as did abnormal heart rate recovery (patients with diabetes: HR, 2.21; 95% CI, 1.60-5.05; P<.001; patients without diabetes: HR, 1.75; 95% CI, 1.55-1.97). CONCLUSIONS: Patients with diabetes exhibit abnormal heart rate responses to exercise, which are independently predictive of reduced long-term survival in patients with diabetes as in patients without diabetes.