Ali Çoner

Which is responsible for cardiac autonomic dysfunction in non-diabetic patients with metabolic syndrome: Prediabetes or the syndrome itself?

AIMS Cardiac autonomic dysfunction (CAD) is associated with both prediabetes and metabolic syndrome (MS). Heart rate variability (HRV) and heart rate turbulence (HRT) are reliable 24-h Holter-ECG findings of cardiac autonomic function. This study aimed to investigate the relation between MS and its components and CAD using HRV and HRT. MATERIALS AND METHODS The study included 80 non-diabetic patients with MS and 70 control subjects. All study population and the patients with MS were further analyzed for each diagnostic component of MS to investigate which criteria impaired HRV and HRT. RESULTS HRV and HRT parameters were disturbed in patients in the MS group. While impairment in HRV and HRT was significantly related to the presence of the fasting plasma glucose (FPG) criterion, there were no differences between groups in terms of the other 4 MS criteria. Moreover, FPG level was significantly correlated with SDNN (r=-0.352, p<0.001), SDNN index (r=-0.423, p<0.001), SDANN (r=-0.301, p<0.001), RMSSD (r=-0.237, p<0.001), pNN50 (r=-0.237, p<0.001), turbulence onset (TO) (r=0.365, p<0.001) and turbulence slope (TS) (r=-0.365, p<0.001). Among the MS diagnostic criteria, only FPG level was an independent determinant of all HRV and HRT parameters. CONCLUSIONS This study confirms the relation between MS and CAD. Increased FPG alone appears to be responsible for the mentioned findings among the 5 diagnostic criteria. Accordingly, CAD may be the result of prediabetes, not MS in patients with MS.

Cardiac autonomic nervous dysfunction detected by both heart rate variability and heart rate turbulence in prediabetic patients with isolated impaired fasting glucose

Objective: Cardiac autonomic nervous dysfunction (CAND), a severe complication of diabetes, has also been shown to affect prediabetic patients. The role of isolated impaired fasting plasma glucose (IFG), a subtype of prediabetes, is not clear in the pathogenesis of CAND. The aim of this study was to examine the relationship between isolated IFG and cardiac autonomic function using heart rate variability (HRV) and heart rate turbulence (HRT) indices derived from 24-h Holter–electrocardiogram recordings. Methods: This observational, prospective, cross-sectional study examined 400 consecutive subjects divided into three groups according to oral glucose tolerance test results: the control group [Group I, fasting plasma glucose (FPG) <100 mg/dL and normal glucose tolerance, n=193], the isolated IFG group (Group II, FPG ≥100 and <126 mg/dL, n=134), and the isolated impaired glucose tolerance (IGT), both IFG and IGT, or newly diagnosed diabetes’ group (Group III, n=73). Patients with non-sinus rhythm, known diabetes mellitus, coronary artery disease, heart failure, severe valvular disease, or receiving medical therapy that may affect HRV and HRT indices were excluded. Time domain HRV parameters, turbulence onset (TO), turbulence slope (TS), and HRT category were examined. Chi-square, one-way analysis of variance, Kruskal–Wallis H, and Mann–Whitney U tests were used to compare variables where appropriate. The correlation between Holter data and FPG levels was analyzed using the Spearman’s test. Multiple linear regression analysis was performed to identify independent predictors of the HRV and HRT parameters. Results: Median (interquartile range 25–75) FPG levels in Groups I, II, and III were 89 (83/93) mg/dL, 109 (104/116) mg/dL, and 174 (150.5/197) mg/dL, respectively. There were significant differences in HRV and HRT parameters between and among all groups. While HRV parameters and TS decreased from Group I to Group III, TO and HRT category gradually increased. Additionally, FPG level was significantly correlated with SDNN, r=–0.220; SDNN index, r=–0.192; SDANN, r=–0.207; RMSSD, r=–0.228; pNN50, r=–0.226; TO, r=0.354; and TS, r=–0.331 (all p<0.001). Conclusion: CAND, as detected by both HRV and HRT, appear to be present in the isolated IFG subtype of prediabetes.

Successful treatment of massive pulmonary embolism with reteplase

Unexpected and unexplained out-of-hospital cardiac arrests have a poor prognosis. Difficulties encountered during the differential diagnosis phase may delay the administration of specific treatment for treatable and reversible causes of cardiac arrest. Massive pulmonary embolism is a reversible cause of cardiac arrest, but without proper management it has a high mortality rate. Presently described is the case of a 53-year-old female patient with a massive pulmonary embolism.

Predictors of neurologically favorable survival among patients with out-of-hospital cardiac arrest: A tertiary referral hospital experience

I read with great interest the original article written by Balcı et al. published in the April 2017 issue of the journal[1] about out-of-hospital cardiac arrest victims and factors predicting neurologically favorable survival. Out-of-hospital cardiac arrests have poor clinical outcomes despite medical improvements, and even with proper cardiopulmonary resuscitation interventions offered in current guidelines, survival rates remain low.[2] With on-going cardiopulmonary resuscitation, it is vital to search for the treatable and reversible causes of cardiac arrest. Physicians should be aware of every clue that may be related to the patient’s collapse. It is a challenging situation to make a differential diagnosis at the time of on-going cardiopulmonary resuscitation and interventions, but some clinical findings can be helpful. As proof of this low rate of definitive diagnosis, Balcı et al. reported 58.1% unknown diagnosis related to out-of-hospital cardiac arrests.[1] Usually, we do not have enough time to correct our possible differential diagnosis, and we have to manage out-of-hospital cardiac arrest patients depending on “most probable differential diagnosis.” This kind of management can direct us to a faster specific treatment choice while cardiopulmonary resuscitation is going on. Initial heart rhythm can give us that kind of chance for management. Balcı et al. reported asystole as initial rhythm on monitor at first sight in 97 of patients out of 129 victims.[1] However, in a recently published paper investigating initial heart rhythm in out-of-hospital cardiac arrest victims, asystole as initial rhythm was reported to be as low as 34%, and even lower in bystander-witnessed cases.[3] This difference in asystole as initial rhythm may be related to prolonged transportation time, as reported in the article by Balcı et al.,[1] and may be even greater case percentage when there is no witness. Yamaguchi et al. also reported that pulseless electrical activity or shockable first rhythm, such as ventricular tachycardia/ventricular fibrillation, has a more favorable clinical outcome.[3] In a report previously published,[4] it was also suggested that initial rhythm can guide physicians in the possible differential diagnosis. In this report, ischemic coronary events were found to be more related to initial rhythms of asystole and ventricular arrhythmias. Interestingly, the authors suggested that witnessed, atraumatic, out-of-hospital cardiac arrest with initial rhythm of pulseless electrical activity is most probably related to massive pulmonary embolism. Also in this paper, the authors claimed that pulseless electrical activity is somehow a neurologically more favorable clinical presentation than other initial rhythms, such as asystole.[4] Physicians and emergency ambulance service medical staff dealing with out-of-hospital cardiac arrest victims should evaluate initial heart rhythm on monitor promptly for possible differential diagnosis and to decide on specific treatment of reversible etiological factors of cardiac arrest. Initial heart rhythm can be a strong predictor of neurological outcome in survivors of out-of-hospital cardiac arrest.

Renal artery stenting of chronic kidney disease patient with resistant hypertension.

Resistant hypertension is a clinical entity presenting with uncontrolled blood pressure (BP) despite use of 3 or more antihypertensive drugs, including diuretic. Reno vascular hypertension related to renal artery stenosis (RAS) occurs in etiology of hypertension and affects up to 5% of all hypertensive patients (1). Fifty-five-year-old male patient was admitted to our clinic with uncontrolled BP. He was using several antihypertensive drugs, including diuretic. He had history of chronic kidney disease and untreated renal artery stenosis. He had residual amount of 500 mL daily urine output. We wanted to evaluate his residual renal function with diuretic administration. We increased daily urine output up to 1500 mL with furosemide and this encouraged us to pursue renal artery intervention. Renal angiography revealed moderate stenosis of right renal artery and severe stenosis of left renal artery. We implanted a 4.0x15 mm bare metal stent in left renal artery. BP responded immediately after intervention and we were able to discontinue antihypertensive drugs. Daily urine output increased up to 1000 mL without diuretic. Hemodialysis sessions were decreased to 2 days per week. RAS primarily causes significant reduction in renal blood flow and is notable factor in development of progressive kidney failure. Atherosclerotic RAS patients present with persistent and progressive reduction in glomerular filtration rate, treatment resistant severe hypertension, and recurrent episodes of flash pulmonary edema. Pathogenesis of chronic kidney disease progression due to RAS is assumed to be more complex than just arterial narrowing. Different cytokines and chemokines related to stimulation of Anatol J Cardiol 2016; 16: 889-96 Letters to the Editor 894

Severe hypocalcemia and hypercalciuria due to contrast medium in the course of acute myocardial infarction

Contrast media-related nephropathy is one of the possible complications in myocardial infarction patients following primary percutaneous intervention (PCI). Contrast media-related nephropathy is mainly defined as a decrease in creatinine clearance and an increase in serum creatinine levels; however, contrast media may also cause electrolyte imbalances. Here we present a case report of severe electrolyte deficiency related with contrast media administration.

[A rare complication of percutaneous coronary intervention: aortic pseudoaneurysm].

On gün önce perkütan koroner girişim (PKG) uygulanmış 74 yaşındaki kadın hasta akut koroner sendrom tanısı ile hastaneye yatırılarak subakut stent trombozuna perkütan balon anjiyoplasti yapıldı. İşlemden birkaç saat sonra sırtından sol omzuna yayılan şiddetli künt ağrı tanımlayan hastanın suprasternal ekokardiyografik incelemesinde inen aort proksimalinde düzensiz sınırlı bir genişleme mevcuttu. Çekilen toraks bilgisayarlı tomografide arkus aorta ile inen aort birleşim yerinde 3 cm çapında ve üst duvarında 1 cm kalınlığa ulaşan trombüs materyalinin izlendiği psödoanevrizmatik genişleme görüldü (Şekil A ve B). Psödoanevrizmanın sol subklavya arterine komşuluğu nedeniyle (Şekil C) endovasküler girişime uygun olmadığına karar verilerek hastaya cerrahi onarım önerildi ancak hasta onam vermediği için yapılamadı. Hastane içi dönemde önemli bir kardiyak ve serebrovasküler istenmeyen olay yaşanmadı. Aort psödoanevrizması intima, medya ve adventisya tabakalarının hasarlanması sonucu oluşan trombüsün aort çevresi bağ dokusu tarafından çevrelendiği aort genişlemesidir. Genellikle künt toraks travmalarına ikincil gelişse de yatrojenik nedenleri arasında kateter aracılı tedaviler de yer alır. Rüptür nedeniyle ani ölüm, fistül oluşumu, çevre dokulara bası ve erozyon gibi hayatı tehdit eden olaylara yol açabilir. Anatomik olarak uygunsa endovasküler ya da cerrahi girişim psödoanevrizmanın boyutundan bağımsız olarak her zaman endikedir. Olgumuzun semptomlarının kateterizasyonundan sonra başlaması ve psödoanevrizmanın lokalizasyonu bu durumun PKG sırasında kılavuz tel ya da kateter travmasına ikincil geliştiğini düşündürmektedir. Zeminde var olabilecek azalmış aort esnekliği, aort enfeksiyonları ya da penetran ülserler kateter aracılı travmayı kolaylaştırmış olabilir. 90

Chronic aortic dissection and recoarctation as a late complication of aortic coarctation surgery.

A 53-year-old female patient was admitted to the outpatient cardiology clinic for control, and described no complaints at admission. She had a history of operation for aortic coarctation 35 years previously with no follow-up in the intervening period. Transthoracic echocardiography, revealed a 50 mmHg peak transaortic gradient at the descending aorta. Thoracic computed tomography (CT) with contrast injection was performed to reveal the aortic anatomy. This showed a giant pseudoaneurysm 94x78 mm in size located at the end of the arch after the level of the recoarcted part to the descending aorta. A chronic dissection flap was also present (Figure A). A 3-D CT image revealed the recoarctation site with pseudoaneurysm (Figure B). Reoperation for chronic aortic dissection and recoarctation was offered. Coarctation of the aorta, a congenital malformation, is generally detected in infancy and sometimes in childhood or early adulthood. Patients with a surgically-repaired aortic coarctation frequently remain asymptomatic for a long period. However, many late complications can occur with aging and some patients may need repeat surgery or reintervention. The median time from coarctation repair to reoperation is 25 years. Because of the silent progression of late complications, careful and close follow-up is needed in patients operated on for aortic coarctation. As seen in the present case, patients may remain entirely asymptomatic for life. We wished to present the CT images of the patient due to the asymptomatic clinical nature of the giant pseudoaneurysm. 752

The Effects of Niacin on Inflammation in Patients with Non-ST Elevated Acute Coronary Syndrome

BACKGROUND In this study, we aimed to evaluate the effects of niacin on high sensitivity C reactive protein (hs-CRP) and cholesterol levels in non-ST elevated acute coronary syndrome (NSTE-ACS) patients. METHODS In this prospective, open label study, 48 NSTE-ACS were randomized to niacin or control group. Patients continued their optimal medical therapy in the control group. In the niacin group patients were assigned to receive extended-release niacin 500 mg/day. Patients were contacted 1 month later to assess compliance and side effects. Blood samples for hs-CRP were obtained upon admittance to the coronary care unit, in the third day and in the first month of the treatment. Fasting blood samples for cholesterol levels were obtained before and 30 days after the treatment. The primary end point of the study was to evaluate changes in hs-CRP, cholesterol levels, short-term cardiovascular events, and the safety of niacin in NSTE-ACS. RESULTS Baseline demographic, clinical and laboratory characteristics were similar between the two groups. Logarithmic transformation of baseline and 3(rd) day hs-CRP levels were similar between the groups; but 1 month later, logarithmic transformation of hs-CRP level was significantly lower in the niacin group (0.43 ± 0.39 to 0.83 ± 0.91, p = 0.04). HDL-C level was significantly increased in the niacin group during follow-up. Drug related side effects were seen in 7 patients in the niacin group but no patients discontinued niacin. CONCLUSIONS Our findings demonstrate that lower dose extended release niacin can be used safely and decreases hs-CRP and lipid parameters successfully in NSTE-ACS patients. KEY WORDS Acute coronary syndrome; hs-CRP; Inflammation; Niacin.

Management of myocardial infarction related to in situ thrombosis.

A 49year old female patient was admitted with anginal complaints accompanied by ST -elevation of 3-4mm in leads V2-V4 of electrocardiogram and diagnosis of acute anterior STEMI was established. Diagnostic coronary angiography revealed an osteal thrombotic stenosis in the left anterior descending artery (LAD) (Fig. 1, Video 1. See corresponding video/movie images at www.anakarder.com). This subtotal occlusive thrombus in the proximal LAD was thought to be the result of endogenous fibrinolysis after total occlusion and the mid occlusion was thought to be due to the embolization from the proximal thrombus. A GP IIb/IIIa blocker tirofiban bolus was given at a dose of 10 microgram/kg IV and both proximal thrombotic lesion and distal occlusion were passed with 0.014 inch floppy wire. Aspiration thrombectomy with Medtronic Export aspiration catheter was performed (Fig. 2). After aspiration thrombectomy, TIMI III flow and a myocardial blush grade (MBG) score of 2 were achieved (Fig. 3, Video 2, 3. See corresponding video/movie images at www.anakarder.com). To be sure, that there was no dissection, but only in-situ thrombus formation intravascular ultrasonography (IVUS) with CromoFlo was performed with Volcano Eagle Eye Gold IVUS catheter (Fig. 4). Therefore, no balloon angioplasty and stent-