instruction:
Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
question:
Many patients with coronary heart disease (CHD) are not managed adequately, and we often fail to reach treatment targets.', 'To investigate if knowledge of risk factors for CHD, measured by a questionnaire, would show any relation to advice to compliance to lifestyle changes to attain treatment goals and adherence to drug therapy.', 'Men and women <71 years who had had a cardiac event were screened consecutively (509) from the medical records. Responders (392) were interviewed, examined and received a questionnaire. Three hundred and forty-seven patients answered the questionnaire regarding their general knowledge of risk factors for CHD, compliance to lifestyle changes to attain treatment goals and adherence to drug therapy.', 'There were statistically significant correlations between general knowledge about risk factors for CHD and compliance to certain lifestyle changes: weight, physical activity, stress management, diet, attainment of lipid level goals and the likelihood of taking prescribed blood pressure-lowering drugs. General knowledge of risk factors had no correlation to blood glucose or blood pressure levels nor on smoking habits or treatment patterns for prescribed lipid- and blood glucose-lowering drugs.
answer:
Does better knowledge improve adherence to lifestyle changes and medication in patients with coronary heart disease?


question:
Angiotensin II (Ang II) signaling has been implicated in cardiac arrhythmogenesis, which involves induction of reactive oxygen species (ROS). It was shown that Ang II can activate Ca/Calmodulin kinase II (CaMKII) by oxidation via a NADPH oxidase 2 (NOX2)-dependent pathway leading to increased arrhythmic afterdepolarizations. Interestingly, cAMP-dependent protein kinase A (PKA) which regulates similar targets as CaMKII has recently been shown to be redox-sensitive as well.', 'This study aims to investigate the distinct molecular mechanisms underlying Ang II-related cardiac arrhythmias with an emphasis on the individual contribution of PKA vs. CaMKII.', 'Isolated ventricular cardiac myocytes from rats and mice were used. Ang II exposure resulted in increased NOX2-dependent ROS generation assessed by expression of redox-sensitive GFP and in myocytes loaded with ROS indicator MitoSOX. Whole cell patch clamp measurements showed that Ang II significantly increased peak Ca and Na current (ICa and INa) possibly by enhancing steady-state activation of ICa and INa. These effects were absent in myocytes lacking functional NOX2 (gp91phox(-/-)). In parallel experiments using PKA inhibitor H89, the Ang II effects on peak INa and ICa were also absent. In contrast, genetic knockout of CaMKIIδ (CaMKIIδ(-/-)) did not influence the Ang II-dependent increase in peak ICa and INa. On the other hand, Ang II enhanced INa inactivation, increased late INa and induced diastolic SR (sarcoplasmic reticulum) Ca leak (confocal Ca spark measurements) in a CaMKIIδ-, but not PKA-dependent manner. Surprisingly, only the increase in diastolic SR Ca leak was absent in gp91phox(-/-)myocytes suggesting that Ang II regulates INa inactivation in a manner dependent on CaMKII- but not on NOX2. Finally, we show that Ang II increased the propensity for cellular arrhythmias, for which PKA and CaMKII contribute, both dependent on NOX2.
answer:
Does nADPH oxidase 2 mediate angiotensin II-dependent cellular arrhythmias via PKA and CaMKII?


question:
We sought to describe the degree of long-term left ventricular (LV) remodeling after acute transmural myocardial infarction with preserved LV systolic function, and to evaluate whether Doppler echocardiographic parameters in the early phase could predict this process.', 'A total of 60 patients without heart failure and with LV ejection fraction > or = 0.40 (mean 0.48 +/- 0.054), were followed up with Doppler echocardiographic examinations at baseline, 3 months, and 1 and 2 years.', 'There was a significant increase in LV end-diastolic volume index of 7% (P =.006) and LV end-systolic volume index of 8% (P =.03), and no change in ejection fraction. This remodeling was confined to 7 patients (12%) with a significant increase in LV end-diastolic volume index above 20 mL/m(2). There was also a significant increase in the deceleration time of both the early mitral filling wave (Delta early mitral filling wave = 58 milliseconds, P <.0005) and the diastolic forward component of pulmonary venous flow (Delta diastolic forward component of pulmonary venous flow = 61 milliseconds, P <.0005), and a shift in filling pattern with increasing prevalence of abnormal relaxation. Changes in end-diastolic volume index were predicted by baseline early mitral filling wave less than 100 milliseconds, but the most powerful predictors of 2-year remodeling were volume changes at 3 months.
answer:

Are early changes in left ventricular volume and function predictors for long-term remodeling in patients with acute transmural myocardial infarction and preserved systolic function?