Bilal Geyik

Myocardial injury due to lightning strike--a case report.

Lightning strike is a natural phenomenon with potentially devastating effects and represents one of the leading causes of cardiac arrest and death from environmental phenomena. Almost every organ system may be impaired as lightning passes through the human body taking the shortest pathways between the contact points. In this paper, the authors report a 38-year-old man who was injured by lightning, a typical example of “side splash,” and had transient electrocardiographic changes.

Copeptin (C-terminal provasopressin): A promising marker of arrhythmogenesis in arrhythmia prone subjects?

Neurohormones have drawn particular attention in the recent years possiblyduetotheirpotentialdiagnosticandprognosticvalues inavarietyof clinical conditions includingcongestiveheart failure(CHF), acutemyocardial infarction (AMI), etc. Among neurohormones, arginine vasopressin (AVP) has been known to be secreted by hypothalamus in response to hypovolemia and increased plasma osmolality [1], and was also demonstrated to be a marker of the presence and severity of CHF [2]. However as described below, the potential association between AVP system and arrhythmogenesis may also confer some important therapeutic and prognostic implications in arrhthmia-prone patients. In the recent years, due to the instability and rapid clerance [1], the clinical utility of AVP has beengraduallyabandonedtosomedegree, andcopeptin(CP), anothernovel neurohormone of the AVP system, has come into use in the clinical practice. CP, the C-terminal portion of provasopressin [1], is co-released with AVP from hypothalamus. CP is structurally more stable, and hence may mirror the stable levels of AVP associated with the severity of the related disease [1]. CP was recently demonstrated to be a strong predictor of mortality and morbidity in patients suffering heart failure after an AMI [1]. In another study [3], CP was found to be associated with left ventricular dysfunction (inverse correlation between copeptin levels and left ventricular ejection fraction (LVEF)) in the early (at discharge) and late stages (on follow-up) of AMI indicating that hyperactivation of the AVPsystemseems tobea contributor (via inducing remodelling) and/or a consequence in the process of heart failure development. However, as an absolute clinical implication inCHF, substantial levels of CPmay indirectly denotepoor systemicperfusionassociatedwithdepressed left ventricular systolic function (a notion consistent with a previous study that demonstrated a negative correlation between AVP and cardiac index [2]). CHF is a well known trigger for malign ventricular arrhythmias through various mechanisms including structural alterations of myocardium, increased myocardial wall tension, adrenergic activation, enhanced effects of the AVP system on the heart, etc. AVP (co-secreted with CP) was suggested to induce protein synthesis, cardiac hypertrophy [4] and collagen synthesis in cardiac fibroblasts [5] in rats that may not only induce myocardial remodelling but may also create an arrhythmogenic substrate for malign ventricular arrhythmias indicating direct arrhythmogenic effects of AVP on myocardium in patients with CHF. It may be suggested that the association between CP levels and arrhythmogenesis may be dependent on left ventricular function, to some extent. However, this association may still persist even after adjustment for parameters of left ventricular function (LVEF, etc.) suggesting CP as an arrhythmogenic marker in arrhythmia-prone patients without heart failure as well. In the absence of heart failure, CP may still remain associated with arrhythmogenesis through various potentialmechanisms: CPwas found to be associatedwith the individual stress level [6]. In a very recently published study, CP was reported to have an additional diagnostic value in AMI (for rapid rule out) as an endogenous stress marker [7]. Hyperactivation of the adrenergic system is generally suggested to trigger malign ventricular arrhythmias and sudden cardiac death (SCD) in arrhythmia-prone subjects [8], and iswell known to be associated with the endogenous stress level. Therefore, CP may be regarded as a promising biochemical marker of arrhythmogenesis in arrhytmia-prone patients with and without heart failure. It may be suggested that besides conventional indices of arrhythmogenesis (QT dispersion, T wave alternance (TWA), heart rate variability (HRV), etc.), clinicians are in need of novel biochemicalmarkers thatmay rapidly and reliably predict the risk for arrhythmogenesis and arrhythmic mortality in arrhythmia-prone patients. CP, the novel and promising marker with strong predictive values, may help predict arrhythmia risk, and may help determine the therapeutic strategy in these patients. However, future large scale studies particularly focusing on the link between arrhythmogenesis and CP in arrhythmia-prone subjects are still warranted to confirm the clinical utility of CP in these patients. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [9].

Does p-wave dispersion predict the atrial fibrillation occurrence after direct-current shock therapy?

Supraventricular tachycardia attacks, including atrial fibrillation (AF), occur after both external and internal cardioversions. These attacks of atrial fibrillation after direct-current (DC) shock may be related to hemodynamic impairment, thromboembolic events, or enhanced electrical instability of the ventricular and atrial myocardium, especially in predisposed patients. In this study, the authors aimed to show the importance of P-wave dispersion (PWD), which lead the atrium to fibrillate, in predicting post-DC shock AF after external cardioversion. Thus physicians may be able to choose the patients with high risk for AF occurrence and apply some other therapeutic modalities to those patients. The authors identified 18 patients in whom an AF attack was induced by urgent or elective cardioversion for a ventricular tachycardia attack and compared these patients with a control group composed of 40 patients without AF in regard to some clinical, echocardiographic, and electrocardiographic parameters. Left atrial diameters were greater (4.3 ±0.3 vs 3.5 ±0.5 cm, p=0.001), left ventricular ejection fractions (LVEF) were lower (45.2 ±8.2 vs 54.9 ±7.5, p=0.001), the energy needed for successful cardioversion was higher (166.6 ±59.4 vs 80.8 ±51.6 J, p=0.001), and P max (135.2 ±7.4 vs 118.7 ±10.5 ms, p=0.001) and PWD (53.8 ±12.2 vs 23.8 ±9.5 ms, p=0.001) values were higher in patients with AF when compared to those without AF. Thus, the patients with higher PWD values had a greater risk for development of AF after a DC shock.

Sympathetic Overactivity in Patients with Rheumatic Mitral Stenosis

Background: Mitral stenosis may increase sympathetic nervous activity by increasing left atrial pressure and reducing cardiac output. And elevated sympathetic nerve activity may be a risk factor for the development of clinical manifestations of mitral stenosis. In this study, we assessed the autonomic nervous system activity in patients with mitral stenosis by heart rate variability analysis and defined factors affecting autonomic functions.

Plasma levels of tumor necrosis factor-α and its receptors in patients with mitral stenosis and sinus rhythm undergoing percutaneous balloon valvuloplasty

This study aimed to determine whether plasma levels of tumor necrosis factor-α (TNF-α) and soluble TNF receptor (sTNF-R) increases in rheumatic mitral stenosis (MS) patients with sinus rhythm and to examine the effect of percutaneous mitral balloon valvuloplasty (PMBV) on these parameters. Twenty-six patients with MS and sinus rhythm (study group, 20 female, mean age 33 ± 8 years), who were scheduled for PMBV, and a well-matched control group consisting of 21 healthy volunteers (15 female, mean age 35 ± 6 years) were enrolled in the study. Tumor necrosis factor-α and sTNF-R levels were compared between study patients and controls, and between peripheral and left atrium (LA) blood. Changes in TNF α and sTNF-R levels 24 h and 4 weeks after PMBV were analyzed. Significantly higher baseline TNF-α and sTNF-R levels were noted in the study group. In the study group, TNF-α and its receptors were also found to be higher in LA blood than in baseline peripheral blood. After PMBV, mitral valve area (MVA) increased and transmitral pressure gradient decreased significantly. At the 24th hour after PMBV, the TNF-α level decreased from 29.61 ± 12.22 pg/ml to 22.42 ± 8.81 pg/ml (P < 0.0001) and at the 4th week, from 22.42 ± 8.81 pg/ml to 18.92 ± 7.37 pg/ml (P < 0.0001). Similar reductions were observed in the sTNF-R level. Regression analysis between the difference in sTNF-R level measured 24 h after and before PMBV and the difference in MVA measured 24 h after and before PMBV showed a significant direct relationship between these variables. This study suggests that isolated rheumatic MS without atrial fibrillation is accompanied by increased TNF-α and sTNF-R level. The successful PMBV establishes a significant reduction in TNF-α and its receptors, probably due to improved postprocedural hemodynamic parameters.

P-Wave Durations in Patients Experiencing Atrial Fibrillation During Exercise Testing

Augmented sympathoadrenal activity during exercise may contribute to occurrence of various arrhythmias including atrial fibrillation (AF). The prolongation of intraatrial and interatrial conduction times and inhomogeneous propagation of sinus impulses are well-known characteristics of the atrium prone to fibrillate and are evaluated by maximum P-wave duration (P max), P-wave dispersion (PWD). To show the increased P max and PWD values in patients experiencing AF during exercise testing and the role of beta blockade on treatment of exercise-induced AF, 22 of these patients were compared with a control group consisting of 41 patients without AF attacks. P max (p=0.001) and PWD (p=0.001) values were significantly higher in patients with AF compared to those without AF. The development of AF during exercise testing was found to be positively correlated with P max (r =0.87, p<0.001), PWD (r =0.83, p=0.001), and work load (r =0.34, p=0.002) and negatively correlated with ejection fraction (r =-0.26, p=0.02). After the treatment with beta-blocking agents for 2 weeks, the decrease in P max and PWD values was accompanied by a much lower prevalence of exercise-induced AF. Consequently, the patients with AF had greater P max and PWD values compared to control subjects, and these simple parameters were well correlated with the occurrence of AF during exercise testing. Furthermore, treatment of these patients with beta blockers would appear to decrease the recurrence of exercise-induced AF and to be associated with a decrease in P-wave durations.

Effect of Cardiac Resynchronization Therapy on Thyroid Function

Heart failure patients frequently have thyroid function abnormalities. Cardiac resynchronization therapy (CRT) is a major treatment for patients with advanced chronic heart failure. We aimed to investigate the effects of CRT on thyroid functions.

Single Coronary Artery Presenting with Cardiogenic Shock due to Acute Myocardial Infarction

Percutaneous coronary revascularization plays an important role in the management of acute coronary syndrome. Unpredictable angiographic findings of anomalous coronary arteries may, however, compromise the otherwise high and predictable success rates of this intervention. We report a case of failed coronary angioplasty of the left anterior descending artery through an anomalous left main coronary artery originating from the right coronary sinus in a 33-year-old man with acute myocardial infarction complicated by cardiogenic shock. Subsequently the patient performed successful emergency coronary artery bypass graft.

Serum level of lipoprotein (a) is inversely associated with the development of coronary collateral circulation

BackgroundThis study sought to determine the relationship between serum lipoprotein (a) levels and angiographically visible coronary collateral circulation and to evaluate whether lipoprotein (a) exerts any effect on vascular endothelial cell growth factor. MethodsThe study population included 60 patients (39 men, mean age 59±13 years) with angiographically documented total occlusion in one of the major coronary arteries. Development of collaterals was classified by Rentrops method. Patients were defined as having poorly developed collaterals for grades 0 and 1 (group 1), or well-developed collaterals for grades 2 and 3 (group 2). Serum lipoprotein (a) and vascular endothelial cell growth factor levels were determined by enzyme-linked immunosorbent assay. ResultsIn group 1, lipoprotein (a) levels were significantly higher and vascular endothelial cell growth factor levels were significantly lower than in group 2 (34±19 vs. 20±12 mg/dl, P<0.001, and 2.5±0.7 vs. 3.4±0.8 ng/dl, P<0.001, respectively). Poorly developed collaterals were significantly more frequent in patients with lipoprotein (a) levels ≥30 mg/dl than in patients with levels <30 mg/dl (72 vs. 37%, P=0.008). A strong negative correlation was observed between lipoprotein (a) and vascular endothelial cell growth, factor (r=−0.708, P<0.0001). Multivariate analysis revealed that a high level of lipoprotein (a) negatively affected the development of collaterals, whereas the duration of angina had a positive effect. ConclusionThis study demonstrated for the first time that the high level of lipoprotein (a) negatively affects the formation of coronary collateral vessels in human beings. Reduced production or bioactivity of vascular endothelial cell growth factor caused by high levels of lipoprotein (a) may be the possible responsible mechanisms of hyperlipoprotein (a)-related poor collateral formation.

Relationship Between Endothelial Functions and Acetylsalicylic Acid Resistance in Newly Diagnosed Hypertensive Patients

We aimed to investigate the effects and dose dependency of aspirin on endothelial functions and prevalence of aspirin resistance in newly diagnosed hypertensive patients without previous drug therapy and development of cardiac complications.