Utility of measuring C-reactive protein for prediction of in-hospital events in patients with acute aortic dissection.

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.

Overexpression of angiotensin-converting enzyme 2 by renin-angiotensin system inhibitors. Truth or myth? A systematic review of animal studies.

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.