Exercise induced increase in diastolic blood pressure. Is it an indicator of coronary artery disease?

1991 ◽  
Vol 12 (11) ◽  
pp. 1195-1197 ◽  
Author(s):  
D. ACANFORA ◽  
L. DE CAPRIO ◽  
A. DI PALMA ◽  
S. PARLATI ◽  
C. LIRATO ◽  
...  
Heart ◽  
1993 ◽  
Vol 69 (6) ◽  
pp. 507-511 ◽  
Author(s):  
I A Paraskevaidis ◽  
D T Kremastinos ◽  
A S Kassimatis ◽  
G K Karavolias ◽  
G D Kordosis ◽  
...  

2019 ◽  
Vol 6 (14) ◽  
pp. 1109-1112
Author(s):  
Kavirayani P. Hemamalini ◽  
Bitra Veera Raghavulu ◽  
Akula Annapurna ◽  
Gadamsetty Rajkumar ◽  
Challapalli Narasimha Raju

2021 ◽  
Author(s):  
Mayuko Harada Yamada ◽  
Kazuya Fujihara ◽  
Satoru Kodama ◽  
Takaaki Sato ◽  
Taeko Osawa ◽  
...  

<b>Aims: </b>To determine associations of systolic blood pressure (SBP) and diastolic blood pressure (DBP) with new-onset coronary artery disease (CAD) or cerebrovascular disease (CVD) according to glucose status. <p><b>Research Design and Methods: </b>Examined was a nationwide claims database from 2008 – 2016<b> </b>on 593,196 individuals. Cox proportional hazards model identified risks of CAD and CVD events among 5 levels of SBP and DBP. </p> <p><b>Results:</b> During the study period 2,240 CAD and 3,207 CVD events occurred. Compared with SBP ≤119 mmHg, which was the lowest quintile of SBP, hazard ratios (HRs) (95% confidence interval) for CAD/CVD in the 4 higher quintiles (120-129, 130-139, 140-149, ≥150 mmHg) gradually increased from 2.10 (1.73 to 2.56)/ 1.46 (1.27 to 1.68) in quintile 2 to 3.21 (2.37 to 4.34)/4.76 (3.94 to 5.75) in quintile 5 for normoglycemia; from 1.39 (1.14 to 1.69)/1.70 (1.44 to 2.10) in quintile 2 to 2.52 (1.95 to 3.26)/4.12 (3.38 to 5.02) in quintile 5 for borderline glycemia; and from 1.50 (1.19 to 1.90)/1.72 (1.31 to 2.26) in quintile 2 to 2.52 (1.95 to 3.26)/3.54 (2.66 to 4.70) in quintile 5 for diabetes. A similar trend was observed for DBP across 4 quintiles (75-79, 80-84, 85-89, ≥90 mmHg) compared with ≤74 mmHg, which was the lowest quintile. </p> <p><b>Conclusions: </b>Results indicated that cardiovascular risks gradually increased with increases in SBP and DBP regardless of the presence of and degree of a glucose abnormality. Further interventional trials are required to apply findings from this cohort study to clinical practice. </p>


2005 ◽  
Vol 46 (1) ◽  
pp. 79-87 ◽  
Author(s):  
Takuro Kubozono ◽  
Akira Koike ◽  
Osamu Nagayama ◽  
Akihiko Tajima ◽  
Tadanori Aizawa ◽  
...  

2018 ◽  
Vol 72 (11) ◽  
pp. 1227-1232 ◽  
Author(s):  
Poghni A. Peri-Okonny ◽  
Krishna K. Patel ◽  
Philip G. Jones ◽  
Tracie Breeding ◽  
Kensey L. Gosch ◽  
...  

Author(s):  
Rainer Malik ◽  
Marios K. Georgakis ◽  
Marijana Vujkovic ◽  
Scott M. Damrauer ◽  
Paul Elliott ◽  
...  

Observational studies exploring whether there is a nonlinear effect of blood pressure on cardiovascular disease (CVD) risk are hindered by confounding. This limitation can be overcome by leveraging randomly allocated genetic variants in nonlinear Mendelian randomization analyses. Based on their association with blood pressure traits in a genome-wide association study of 299 024 European ancestry individuals, we selected 253 genetic variants to proxy the effect of modifying systolic and diastolic blood pressure. Considering the outcomes of incident coronary artery disease, stroke and the combined outcome of CVD, linear and nonlinear Mendelian randomization analyses were performed on 255 714 European ancestry participants without a history of CVD or antihypertensive medication use. There was no evidence favoring nonlinear relationships of genetically proxied systolic and diastolic blood pressure with the cardiovascular outcomes over linear relationships. For every 10-mm Hg increase in genetically proxied systolic blood pressure, risk of incident CVD increased by 49% (hazard ratio, 1.49 [95% CI, 1.38–1.61]), with similar estimates obtained for coronary artery disease (hazard ratio, 1.50 [95% CI, 1.38–1.63]) and stroke (hazard ratio, 1.44 [95% CI, 1.22–1.70]). Genetically proxied blood pressure had a similar relationship with CVD in men and women. These findings provide evidence to support that even for individuals who do not have elevated blood pressure, public health interventions achieving persistent blood pressure reduction will be of considerable benefit in the primary prevention of CVD.


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