Controlling blood pressure is essential for prevention of events after acute aortic dissection (AAD). However, in some instances a cardiac event occurs despite controlled blood pressure, and its prediction is difficult. We continuously monitored C-reactive protein (CRP) in patients receiving medical treatment for AAD and retrospectively examined the utility of CRP measurement for prediction of in-hospital events. Five hundred and eight patients were diagnosed as having AAD between 1993 and 2009, 240 of whom underwent antihypertensive medical therapy. These subjects were 156 males and 84 females, average age 67.4 years, with 68 cases of Stanford type A and 172 cases of Stanford type B. C-reactive protein was measured in all patients daily until a peak; subsequently, CRP was measured 2-3 times per week following the peak until discharge. In the event-free group CRP demonstrated a peak on the 4th day after the onset (average 13.7 mg/dl), then gradually decreased to an average of 4.6 mg/dl 4 weeks later, displaying a "gradual decay" pattern. Despite controlled systolic arterial pressure of approximately 120 mmHg, 7 of 68 Stanford A cases (10.3 %) and 8 of 172 Stanford B cases (4.7 %) developed cardiovascular events. The group characterized by events exhibited a CRP pattern distinct from that of the event-free group, i.e., prolonged elevation and/or re-elevation. We demonstrated that the CRP pattern could provide information regarding prediction of cardiovascular events. Prolonged elevation or re-elevation of CRP may indicate the necessity of (1) application of computed tomography or magnetic resonance imaging, (2) more rigorous blood pressure management, or (3) early surgical intervention.
Angiotensin-converting enzyme 2 (ACE2) protects against organ damage in hypertension and cardiovascular diseases by counter regulating the renin-angiotensin system (RAS). ACE2 is also the receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Based on the claim that RAS inhibitors (RASIs) cause ACE2 overexpression in some animal experiments, concerns have arisen that RASIs may aggravate SARS-CoV-2 infection and coronavirus disease-2019 severity in RASI-treated patients. To achieve a comprehensive review, a systematic search of MEDLINE/PubMed was conducted regarding the effects of RASIs on tissue ACE2 mRNA/protein expression in healthy animals and animal models of human diseases. We identified 88 eligible articles involving 168 experiments in the heart, kidneys, lungs, and other organs. Three of 38 experiments involving healthy animals showed ACE2 expression greater than twice that of the control (overexpression). Among 102 disease models (130 experiments), baseline ACE2 was overexpressed in 16 models (18 experiments) and less than half the control level (repression) in 28 models (40 experiments). In 72 experiments, RASIs did not change ACE2 levels from the baseline levels of disease models. RASIs caused ACE2 overexpression compared to control levels in seven experiments, some of which were unsupported by other experiments under similar conditions. In 36 experiments, RASIs reversed or prevented disease-induced ACE2 repression, yielding no or marginal changes. Therefore, ACE2 overexpression appears to be a rare rather than common consequence of RASI treatment in healthy animals and disease models. Future studies should clarify the pathophysiological significance of RASI-induced reversal or prevention of ACE2 repression in disease models.
BackgroundLong‐chain fatty acids are essential components of the cellular energy supply, cellular membranes, and autacoid synthesis. It has been suggested that long‐chain fatty acids might be involved in the pathophysiology underlying sarcopenia. We investigated the association between sarcopenia and serum long‐chain fatty acid profile in patients with cardiovascular diseases.MethodsWe retrospectively investigated 308 cardiovascular patients [age: 72 ± 12 (mean ± SD), 174 male patients] admitted to our hospital. All patients were evaluated by sarcopenia diagnostic tests and serum free fatty acid analyses.ResultsSeventy‐seven patients (25%) were diagnosed with sarcopenia. Serum fatty acid weight percentages of nervonic acid and erucic acid were elevated in patients with sarcopenia compared with those without. Nervonic acid, which was an independent factor for sarcopenia in binary logistics regression analysis (B = 2.559, p < 0.001), correlated negatively with skeletal muscle index (r = −0.331, p < 0.001), gait speed (r = −0.387, p < 0.001), and handgrip strength (r = −0.372, p < 0.001). These significant relationships were confirmed in subgroup analyses stratified by age and gender. In receiver operating characteristic curve analysis, the cut‐off of nervonic acid weight percentage for diagnosis of sarcopenia was 1.37% with a sensitivity and specificity of 76.6% and 65.1%, respectively.ConclusionsNervonic acid, an n‐9 monounsaturated fatty acid, might serve as a new marker for sarcopenia in patients with cardiovascular diseases. Further studies with larger patient numbers will be needed to determine the roles of long‐chain fatty acids in sarcopenia.
6. Hildrum B, Mykletun A, Holmen J et al. Effect of anxiety and depression on blood pressure: 11-year longitudinal population study. Br J Psychiatry 2008;193:108-113. 7. Paterniti S, Verdier-Taillefer MH, Geneste C et al. Whether high serum NAG activity would be a predictor of cerebro-and cardiovascular death was examined in a community-based cohort study. Serum NAG activity was measured in 1,070 apparently healthy participants (aged ! 20; 461 male, 609 female) in 1982 using a colorimetric method using an artificial substrate (NAG Test Shionogi). 5,6 Participants were periodically followed up for 28 years (follow-up rate 96.1%.) There were 410 (205 men, 205 women) deaths. Cause of death was cancer in 103 (25.1%) participants, cerebro-or cardiovascular disease (CVD) in 92 (22.4%), infection in 58 (14.1%), dementia in 58 (14.1%), and other causes in 99 (24.1%). Serum NAG activity was categorized into quartiles ( 10.0 IU/L (n = 268), 10.0-12.0 IU/L (n = 268), 12.1-14.0 IU/L (n = 268), and >14.0 IU/L (n = 266)). Baseline serum NAG activity was significantly associated with age, body mass index, blood pressure, total cholesterol, highdensity lipoprotein cholesterol, triglycerides, renal function, uric acid, fasting plasma glucose, medication for hypertension, and all-cause death but not cerebro-or cardiovascular death. Cox proportional hazard regression analysis demonstrated that serum NAG activity was an independent predictor of all-cause death (hazard ratio (HR) = 1.02; 95% confidence interval (CI) = 1.00-1.04, P = .01 per 1-IU/L difference). The HR of all-cause death in the highest quartile of serum NAG ( ! 14.0 IU/L) versus the lowest quartile, after adjustment for confounding factors, was 1.35 (95% CI = 1.02-1.83). Figure 1 shows the Kaplan-Meier curves for cumulative survival rate stratified according to NAG quartile. A significant difference (P < 001) was found, and the highest all-cause mortality was observed in the fourth quartile.Thus, serum NAG activity was an independent and significant predictor of all-cause death. Although high serum NAG activity was associated with all-cause death, the causal relationship was not delineated. Because serum NAG activity is associated with many cardiovascular risk factors and because high serum NAG activity was reported in individuals with cancer, 7-10 it was thought that it might be a predictor of cardiovascular or cancer death, but this was not found to be the case. There may be several reasons for the negative associations, the most likely being that the predictive power was not great enough for statistical analyses.The strength of the present study is that it is the first and the largest and longest prospective cohort study to show that serum NAG is a predictor of all-cause mortality in apparently healthy subjects. The limitations of the present study are that, although every effort was made to collect information about causes of death, it was not possible to clarify cause of death in all subjects because of the extended length of the follow-up period; that only a si...
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