We observed that excess circulating inflammation markers, being characteristic of unstable coronary artery disease, are released from noncoronary sources. Thus, it may be speculated that systemic inflammation precedes local inflammation at the plaques, thereby transforming coronary disease from a stable to an unstable form.

Rapid atrial rates cause electrical, structural remodeling, and neuro-humoral changes. This study compares the effects of mechanical remodeling on plasma renin activity (PRA) and atrial natriuretic peptide (ANP) secretion. Eight beagles were subjected to rapid atrial pacing (AP) at 400 beats/min for 16 days. After complete recovery of left ventricular function, they underwent rapid ventricular pacing (VP) at 240 beats/min of equal duration. Left atrial systolic maximal dimension (LAmax) and left atrial appendage (LAA) peak late emptying velocity (LAA-E) were assessed by echocardiography. Blood samples were taken from the right atrium and from the peripheral vein. LAmax after AP and VP enlarged significantly (2.16 +/- 0.21 cm vs 2.41 +/- 0.23 cm, P = 0.002). Compared with baseline, LAA-E velocities were significantly reduced (0.65 +/- 0.12 m/s vs 0.26 +/- 0.16 m/s, P = 0.001) after AP only. AP caused a significant elevation of PRA in right atrial (9.28 +/- 4.23 nmol/L per hour) and peripheral samples compared with baseline values (4.82 +/- 2.53 nmol/L per hour, P = 0.04). ANP levels increased after AP (1117.12 +/- 252.21 fmol/L) with respect to baseline values (824.37 +/- 159.08 fmol/L, P = 0.001). There was no difference in PRA and ANP levels between atrial and peripheral samples. Atrial size and impaired systolic appendage function play an important role in secretion of PRA and ANP. Both neuro-humoral pathways may be therapeutic targets in the treatment of patients with AF.

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Introduction Aortic stenosis characterization in patients with low flow – low gradient stenosis (LF-LG) and reduced left ventricular (LV) ejection fraction (EF) is challenging. In this subgroup, pseudo- severe stenosis should be properly identified, as these patients are treated conservatively with heart failure therapy. Its identification relies mainly on preserved contractile reserve seen during dobutamine echocardiography. We present a patient with low contractile reserve and pseudo-severe stenosis due to mechanical dyssynchrony. Case presentation 83-years old patient with ischemic heart disease and chronic kidney disease was admitted to our department due to progressive exertional dyspnea. In 2014 he underwent dual-chamber pacemaker (PM) implantation due to sick sinus syndrome and was programmed to asynchronous pacing mode (VVI mode) in 2016 as atrial electrode dysfunction was observed. Coronary angiogram was normal. Echocardiography showed enlarged left ventricle (LV EDV 180 ml), reduced EF (33%) and signs of mechanical dyssynchrony. Peak aortic valve velocity was 2.5 m/s, mean pressure gradient (MPG) 13 mmHg and AVA 1.0 cm2. Stroke volume was reduced (SVI 28 ml/m2). LF-LG aortic stenosis was suspected. Stress echocardiography using dobutamine at peak infusion of 15 mcg/kg/min showed low contractile reserve (EF 37%, SVI 33 ml/m2) with no significant changes in aortic valve parameters (MPG 29 mmHg, AVA 0.9 cm2). However, significant masurement disparity was noted and at least partly contributed to atrio-ventricular (A-V) and inter-ventricular dyssynchrony because of asynchronous VVI pacing. To overcome A-V and intraventricular dyssynchrony we decided for atrial lead reposition and upgrade to cardiac resynchronization therapy (CRT-P). After six months of CRT, normalization of EF and improvement of exercise capacity were observed. Furthermore, additional evaluation of aortic valve showed only moderate stenosis (peak velocity 2,8 m/s, MPG 18 mmHg and AVA 1.4 cm2). Stroke volume was normal (SVI 48 ml/m2). Consequently, we postponed potential surgical or interventional treatment of the aortic valve. Conclusion Considerable LV mechanical dyssynchrony could interfere with determining the severity of aortic stenosis. As demonstrated in the present case report, special considerations should be taken in patients with notable LV dyssynchrony and low contractile reserve as it may not be overcome with dobutamine stress echocardiography as recommended by the current guidelines.