Paricalcitol counteracts the increased contrast induced nephropathy caused by renin-angiotensin-aldosterone system blockade therapy in a rat model.

OBJECTIVE: The effect of vitamin D and renin-angiotensin-aldosterone system blockade medications in pathophysiology of contrast induced nephropathy (CIN) is controversial. The effects of paricalcitol (active vitamin D analogue) and losartan treatments in an experimental model of CIN were investigated in this study. MATERIALS AND METHODS: Thirty-six male Wistar albino rats were examined in five treatment groups. Placebo group (Group A; n = 4) received no active medication; control group (Group B; n = 8) received only contrast media (CM); Group C (n = 8) received paricalcitol; Group D (n = 8) received losartan and Group E (n = 8) received paricalcitol plus losartan. CIN was induced by NG-nitro-L-arginine methyl ester and indomethacin before iohexol injection. Renal histopathological findings were categorized and renal immunohistochemical examinations by caspase-3 rabbit primary antibody were performed. RESULTS: Creatinine and cystatin C levels significantly increased in the treatment groups, compared to Group A. However, creatinine levels were not significantly increased in Groups C, D and E compared to Group B. Compared to Group B, a significant increase of cystatin C levels was observed in Group D (p < 0.01). In Group E, when paricalcitol treatment was added to losartan treatment, cystatin C levels were similar to Group B (p = 1.00). In histopathological and immunohistochemical examination frequency of Grade 2/3 tubular necrosis and renal caspase 3 activity scores were significantly higher in the losartan treatment group compared to the other treatment groups. The histopathological effects related to losartan treatment were found to be reversed when paricalcitol treatment was combined. CONCLUSIONS: Our findings suggest that paricalcitol treatment counteracts increased contrast induced nephropathy caused by losartan. These findings warrant further clinical studies to investigate the benefit of paricalcitol in CIN prophylaxis.

The relationship between antibeta 2 glycoprotein antibodies and SYNTAX score in patients undergoing coronary artery by-pass graft surgery.

OBJECTIVE: The SYNTAX Score was recently developed to characterize the coronary vasculature with respect to the number of lesion's location, complexity, and functional impact and it is a quantitative scoring system to assist with patient selection for optimal revascularization strategy between percutaneous coronary intervention (PCI) and coronary artery by-pass surgery (CABG). b2-glycoprotein I (b2GPI), a plasma protein that binds cardiolipin, acts as a modulator of platelet aggregation and coagulation. Antibodies to b2GPI may have a role in atherosclerosis by inducing endothelial cell activation. We investigated the relationship between anti beta 2 GPI and severity of coronary artery stenosis by calculating the SYNTAX Score among patients undergoing CABG surgery. PATIENTS AND METHODS: We prospectively investigate 612 patients who undergo elective coronary angiography between September 2012 and June 2013. Patients were evaluated for blood chemistry and anti-b2GPI IgA, IgM and IgG. Ninety seven patients with complete biochemical analysis including anti Beta 2 GPI antibodies and undergone CABG have been enrolled in this study. We divided patients in to 2 groups according to the SYNTAX scores. Group 1 included 48 patients with low SYNTAX scores (<23) and group 2 included 49 patients with intermediate and high SYNTAX scores (>23). RESULTS: There was significant correlation between elevated anti b2GPI IgG levels and higher SYNTAX score which indicate advanced and complex CAD. In this study, lesion complexity increased progressively with increasing anti-b2GPI-IgG type of antibody levels. According to this findings, anti-b2GPI-IgG is a strong predictor of higher SYNTAX score. CONCLUSIONS: In addition to the traditional risk factors for atherosclerosis, the proinflammatory and procoagulant activities of antiphospholipid antibodies appear to be important risk factors for atherosclerotic occlusive disease.

Phaeochromocytoma-induced myocarditis mimicking acute myocardial infarction.

A 44-year-old woman presented with sudden onset of chest pain, headache and nausea. Physical examination was remarkable for mild hypotension and tachycardia. ECG demonstrated sinus tachycardia with poor R wave progression in precordial leads and T wave inversion in leads V1-3. Cardiac enzymes were raised. Echocardiographic examination revealed normal cavity diameters with basal and mid left ventricular hypokinesia and an ejection fraction of 45%. A diagnosis of non-ST elevation myocardial infarction was made. A few orthostatic hypotensive attacks occurred at follow-up. A coronary angiogram showed normal coronary arteries. Within a few days, the echocardiographic findings, ECG and all cardiac markers had returned to normal. Two months later she presented with headache, palpitation, fever, neck swelling, flushing and hypertensive attacks. Phaeochromocytoma was diagnosed on the basis of increased metanephrine on urinalysis and a left suprarenal mass on CT scan.

Incessant monomorphic ventricular tachycardia during febrile illness in a patient with Brugada syndrome: fatal electrical storm.

A 55-year-old male with structurally normal heart presented with sustained monomorphic ventricular tachycardia (VT) and was cardioverted into sinus rhythm revealing a right bundle branch block pattern at baseline electrocardiography. Sustained monomorphic and nonsustained polymorphic VT were reproducibly inducible during electrophysiological study. During the diagnostic workup, the patient experienced fever due to hospital based pneumonia, which unmasked typical ST segment changes of Brugada syndrome. In the intensive care unit, fever became intractable leading to incessant monomorphic VT, which was resistant to all medical manoeuvers resulting in the patient's death.

New Doppler echocardiographic applications for the evaluation of early alterations in left ventricular diastolic function after coronary angioplasty.

AIMS: The early effect of percutaneous transluminal coronary angioplasty on left ventricular diastolic dysfunction was investigated with the aid of new Doppler echocardiographic applications. METHODS: Thirty patients with isolated severe left anterior descending coronary artery stenosis were included. All patients exhibited abnormal diastolic function demonstrated by prolonged isovolumic relaxation and deceleration time and decreased E/A ratio. New Doppler indexes included the flow propagation velocity of E wave, E and A waves' transit time to the left ventricular outflow tract, the ratio of these transit times in addition to the traditional isovolumic relaxation time, mitral deceleration time, and early and late transmitral peak flow velocities. All measurements were performed within 4 h before angioplasty and repeated within 24 h after the procedure. RESULTS: After angioplasty none of these parameters, except the A-wave transit time, were changed significantly. The A-wave transit time increased significantly from 57 +/- 5 ms to 78 +/- 7 ms within 24 h after successful angioplasty. The ratio of E- and A-wave transit time decreased significantly due to this significant increase in A-wave transit time. CONCLUSION: In this study, early improvement of Doppler index of left ventricular diastolic compliance is demonstrated after successful angioplasty.