Management of thoracic aortic aneurysms (TAAs) comprises regular diameter follow-up until the indication criterion for prophylactic surgery is reached. However, this approach is unable to predict the majority of acute type A aortic dissections (ATAADs). The current study aims to evaluate the diagnostic accuracy of ascending aortic diameter, length and volume for occurrence of ATAAD.This two-centre observational cohort study retrospectively screened 477 consecutive patients who presented with ATAAD between 2009 and 2018. Of those, 25 (5.2%) underwent CT angiography (CTA) within 2 years before dissection onset. Aortic diameter, length and volume of these patients ('pre-ATAAD') were compared with those of TAA controls (n=75). Receiver operating curve analysis was performed to evaluate the predictive accuracy of the three different measurements.96% of patients with pre-ATAAD did not meet the surgical diameter threshold of 55 mm before dissection onset. Maximal aortic diameters (45 (40-49) mm vs 46 (44-49) mm, p=0.075) and volume (126 (95-157) cm3 vs 124 (102-136) cm3, p=0.909) were comparable between patients with pre-ATAAD and TAA controls. Conversely, ascending aortic length (84±9 mm vs 90±16 mm, p=0.031) was significantly larger in patients with pre-ATAAD. All three parameters had an area under the curve of >0.800. At the 55 mm cut-off point, the maximal diameter yielded a positive predictive value (PPV) of 20%. While maintaining same specificity levels, measurements of aortic volume and length showed superior diagnostic accuracy (PPV 55% and 70%, respectively).Measurements of aortic volume and length have superior diagnostic accuracy compared with the maximal diameter and could improve the timely identification of patients at risk for ATAAD.
Abstract The maximum aortic diameter is the main risk predictor for type A acute aortic syndromes and understanding the growth rate of ascending thoracic aortic aneurysms (aTAAs) is pivotal for risk assessment and stratification for pre-emptive aortic surgery. Prevailing guidelines recommend serial imaging of aTAA patients until the thresholds for prophylactic surgery are met. Based on early landmark studies, it was thought that the growth rate of aTAAs is substantially higher than that of the normal-sized aorta. However, more recent studies have reported that aTAA growth is generally slow, questioning the need for frequent imaging during follow-up. The current systematic review provides an overview of studies reporting annual diameter growth rates of non-syndromic aTAAs and explains differences in findings between early and recent studies.
Management of patients with acute chest pain remains challenging. Cardiac biomarker testing reduces the likelihood of erroneously discharging patients with acute myocardial infarction (AMI). Despite normal contemporary troponins, physicians have still been reluctant to discharge patients without additional testing. Nowadays, the extremely high negative predictive value of current high-sensitivity cardiac troponin (hs-cTn) assays challenges this need. However, the decreased specificity of hs-cTn assays to diagnose AMI poses a new problem as noncoronary diseases (eg, pulmonary embolism, myocarditis, cardiomyopathies, hypertension, renal failure, etc) may also cause elevated hs-cTn levels. Subjecting patients with noncoronary diseases to unnecessary pharmacological therapy or invasive procedures must be prevented. Attempts to improve the positive predictive value to diagnose AMI by defining higher initial cutoff values or dynamic changes over time inherently lower the sensitivity of troponin assays. In this review, we anticipate a potential changing role of noninvasive imaging from ruling out myocardial disease when troponin values are normal toward characterizing myocardial disease when hs-cTn values are (mildly) abnormal.
Left ventricular (LV) hypertrophy and myocardial infarction play important roles in the progressive LV dysfunction. We hypothesized that the potassium-channel opener and nitrate-like vasodilator nicorandil prevents the development of LV hypertrophy and preserves myocardial viability. Twenty-four rats were subjected to aortic stenosis for 8 weeks to produce LV hypertrophy and assigned to non-treated and nicorandil-treated (3 mg/kg/d) groups. A third group (n = 12) without stenosis or treatment served as control. All 36 animals were subjected to reperfused infarction by 25-minute occlusion of the left coronary artery followed by 3 hours of reperfusion. Spin-echo magnetic resonance (MR) images were acquired to measure infarction size, LV mass, volumes, ejection fraction, and wall thickness. A necrosis-specific contrast agent, Gadophrin-3, was used to delineate necrotic myocardium. Aortic and LV pressures were measured invasively. At postmortem, LV mass and infarction size were determined and compared with MR findings. Nicorandil prevented the development of LV hypertrophy. Infarction size of nicorandil-treated animals was similar to control animals. Non-treated animals with aortic banding had higher LV mass (P < 0.001), lower ejection fraction (P = 0.006), and larger infarction size (P < 0.001) than treated and control animals. MR and postmortem data showed close agreement. Nicorandil therapy prevented the development of cardiac hypertrophy and protected myocardium against ischemia.
BASIK2 is a prospective, double-blind, randomized placebo-controlled trial investigating the effect of vitamin K2 (menaquinone-7;MK7) on imaging measurements of calcification in the bicuspid aortic valve (BAV) and calcific aortic valve stenosis (CAVS). BAV is associated with early development of CAVS. Pathophysiologic mechanisms are incompletely defined, and the only treatment available is valve replacement upon progression to severe symptomatic stenosis. Matrix Gla protein (MGP) inactivity is suggested to be involved in progression. Being a vitamin K dependent protein, supplementation with MK7 is a pharmacological option for activating MGP and intervening in the progression of CAVS. Forty-four subjects with BAV and mild-moderate CAVS will be included in the study, and baseline