In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[Q]: Context: Symptomatic patients with severe aortic stenosis (AS) demonstrate abnormal left ventricular (LV) mechanics. The aim of this study was to compare mechanics in asymptomatic and symptomatic patients with severe AS using two-dimensional myocardial strain imaging.', 'One hundred fifty-four patients with severe AS (aortic valve area 1.0 cm(2)) referred to a heart valve clinic from 2004 to 2011 were studied. Thirty patients were asymptomatic, with normal LV ejection fractions ( 55%), without other significant valvular disease or wall motion abnormalities. Thirty-two symptomatic patients who underwent early aortic valve replacement, with similar age, gender, LV ejection fraction, and aortic valve area, were selected for comparison. Both groups were also compared with 32 healthy subjects with similar age and gender distributions and normal echocardiographic results who served as controls. LV longitudinal and circumferential strain and rotation were measured using speckle-tracking software applied to archived echocardiographic studies. Conventional echocardiographic and myocardial mechanical parameters were compared among the study subgroups.', 'Patients with asymptomatic severe AS demonstrated smaller reductions in longitudinal strain, higher (supernormal) apical circumferential strain (-38 6% vs -35 4%, P < .05), and extreme (supernormal) apical rotation (12.2 4.9 vs 2.9 1.7, P < .0005) compared with symptomatic patients. Apical rotation < 6 was the single significant predictor of symptoms in logistic regression analysis of clinical, echocardiographic, and mechanical parameters. Twelve asymptomatic patients underwent eventual aortic valve replacement and showed decreases in strain and apical rotation compared with baseline values.\Question: Are symptoms in severe aortic stenosis associated with decreased compensatory circumferential myocardial mechanics?
[A]: Longitudinal strain was uniformly low in patients with severe AS and lower in those with symptoms. Compensatory circumferential myocardial mechanics (increased apical circumferential strain and rotation) were absent in symptomatic patients. Thus, myocardial mechanics may help in the follow-up of patients with severe AS and timing of valve surgery.

[Q]: Context: Increased triglyceride (TG) occurs in patients with acute coronary syndrome (ACS), and apolipoprotein AV (apoAV) has been shown to lower TG levels. In the present study, we investigated plasma apoAV level and its relationship with TG and C-reactive protein (CRP) in ACS patients.', 'A total of 459 subjects were recruited and categorized into control group (n = 116), stable angina (SA) group (n = 115), unstable angina group (n = 116) and acute myocardial infarction group (n = 112). Plasma apoAV level was measured by a sandwich ELISA assay.', 'Compared with controls ((100.27 +/- 22.44) ng/ml), plasma apoAV was decreased in SA patients ((76.54 +/- 16.91) ng/ml) but increased in patients with unstable angina ((330.89 +/- 66.48) ng/ml, P < 0.05) or acute myocardial infarction ((368.66 +/- 60.53) ng/ml, P < 0.05). Inverse correlations between apoAV and TG were observed in the control or stable angina groups (r = -0.573 or -0.603, respectively, P < 0.001), whereas positive correlations were observed in the patients with unstable angina or acute myocardial infarction (r = 0.696 or 0.690, respectively, P < 0.001). Furthermore, a positive relationship between apoAV and CRP was observed in the ACS patients but not in the non-ACS subjects.\Question: Is elevated plasma apolipoprotein AV in acute coronary syndrome positively correlated with triglyceride and C-reactive protein?
[A]: The plasma apoAV concentration is increased and positively correlates with TG and CRP in ACS patients.

[Q]: Context: Apoptosis occurring during ischaemia /reperfusion contributes independently to tissue damage, and involves activation of the stress-kinase, p38 MAPK during reperfusion. Ischaemic preconditioning (IPC) protects against ischaemia/reperfusion mediated necrosis and apoptosis. The role of p38 MAPK in the protective effect of preconditioning against apoptosis is unknown. Pharmacologic preconditioning with isoproterenol (beta-PC) also protects against necrosis, but it is not known whether it protects against apoptosis.', 'The aim of the study was to investigate whether the protective effect of IPC against apoptosis is related to activation of p38 MAPK and whether beta-PC also protects against apoptosis.', 'Isolated perfused rat hearts were used to study the effect of ischaemia and reperfusion on apoptosis and infarct size. Ischaemic preconditioning was elicited by 3 x 5 min global ischaemia, and beta-PC by 5 min isoproterenol 10(-7) M. For infarct size hearts were subjected to regional ischaemia for 35 min followed by 120 min reperfusion. Infarct size was determined by the tetrazolium staining technique, and expressed as percentage of area at risk. For markers of apoptosis hearts were subjected to global ischaemia of 25 min plus 30 min reperfusion. Apoptosis was determined by Western blot using antibodies against caspase-3 and PARP. p38 MAPK activation was inhibited by SB203580 (1 microM) administration 10 min prior to commencing ischaemia, and bracketing the IPC and beta-PC preconditioning protocols. p38 MAPK was activated by administration of anisomycin (5 microM) 10 min prior to index ischaemia in one protocol, and 10 min during reperfusion in non-preconditioned as well as IPC and beta-PC hearts. Results were analysed using ANOVA and a Newman-Keuls post-hoc test.', 'In the apoptosis model using global ischaemia, IPC and beta-PC both resulted in a significant decrease in p38 MAPK activation at the end of reperfusion when compared to non-preconditioned hearts. This was accompanied by a significant decrease in apoptosis as measured with both caspase-3 activation and PARP cleavage. Inhibiting p38 MAPK by administration of SB203580 10 min prior to ischaemia resulted in a significant reduction in both markers of apoptosis. Bracketing the triggering phase of either IPC or beta-PC with SB203580 resulted in attenuated p38 MAPK activation during reperfusion and did not abolish the protective effect of IPC or beta-PC against apoptosis. Activating p38 MAPK with anisomycin prior to ischaemia resulted in a reduction of markers of apoptosis, whereas activation of p38 MAPK with anisomycin during reperfusion did not exacerbate apoptosis in any groups, exept for an increase in PARP cleavage in IPC hearts. In the model of regional ischaemia, IPC and beta-PC reduced infarct size significantly, and to the same extent as inhibition of p38 MAPK by administration of SB203580 10 min prior to ischaemia. Bracketing the triggering phase of either IPC or beta-PC did not abolish the reduction in infarct size. Activating p38 MAPK during reperfusion was accompanied by an increase in infarct size only in IPC hearts, but not in beta-PC hearts.\Question: Is inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning dependent on p38 MAPK?
[A]:
These results indicate that (1) Both IPC and beta-PC elicit protection against apoptosis and necrosis, (2) activation of p38 MAPK is not a trigger of preconditioning against apoptosis and necrosis and (3) activation of p38 MAPK during reperfusion increases necrosis only if ischaemia is used to precondition hearts, but not with pharmacologic preconditioning with isoproterenol.