Mehmet Akif Cakar

Relation between the GRACE score and severity of atherosclerosis in acute coronary syndrome

BACKGROUND Patients with non-ST-elevation acute coronary syndrome are heterogeneous in terms of clinical presentation and immediate- and long-term risk of death or non-fatal ischemic events. The aim of the present study was to evaluate the relationship between the Global Registry of Acute Coronary Events (GRACE) score and severity of coronary artery disease angiographically evaluated by Gensini score in patients with non-ST-elevation acute coronary syndrome. METHODS A total of 245 patients with non-ST-elevation acute coronary syndrome were enrolled to the study. Based on the GRACE risk score classification system, the patients were divided into low- (n=97, 39.6%), intermediate- (n=84, 34.3%), and high- (n=64, 26.1%) risk groups. All patients underwent coronary angiography within five days after admission. RESULTS The Gensini scores were 26±29 in the low-risk group, 29±19 in the intermediate-risk group, and 38±23 in the high-risk group (p=0.016). The low-risk group was significantly different from the high-risk group (p=0.013), and the difference from the intermediate-risk group almost reached significance. Normal, noncritical, one and two, or multivessel disease were identified in 15 (6.1%), 31 (12.7%), 75 (30.6%), and 124 (50.6%) patients, respectively. The prevalence of multivessel disease was 28% in the low-risk group, 30% in the intermediate-risk group, and 42% in the high-risk group. The high-risk group was significantly different from the low-risk group (p<0.01). CONCLUSION Our study demonstrates that the GRACE score has significant value for assessing the severity and extent of coronary artery stenosis in patients with non-ST-elevation acute coronary syndrome.

Slow ventricular response atrial fibrillation related to mad honey poisoning.

Mad honey poisoning which is induced by Grayanotoxin (Andromedotoxin), is also known to have adverse effects in the cardiovascular system leading to different clinical entities. This toxin is produced by a member of the Rhododendron genus of plants of two R. Luteum and R. Panticum. In this article, we presented a case of slow ventricular response atrial fibrillation complaints with nausea, vomiting, dizziness and chest pain about an hour after eating honey produced in the Black Sea Region.

A delayed diagnosis of a retained guidewire during central venous catheterisation: a case report and review of the literature.

Central venous catheterisation allows delivery of medications, intravenous fluids, parenteral nutrition, haemodialysis and monitoring of haemodynamic variables. Various complications may occur during and after the procedure. However, the complete guidewire retention has rarely been reported. In this report, we have presented a complete guidewire retention as a result of inadvertent catheter insertion. After 17 months of the first operation performed upon the diagnosis of Fourniers gangrene, the patient was admitted to the cardiology polyclinic with a recurrent chest pain. Echocardiography showed a wire-shaped foreign body within the right part of the heart, and a fluoroscopic examination showed a guidewire reaching from the superior vena cava to the right external iliac vein. In retrospect, the wire was already visible on the postoperative chest x-rays and CT taken while the patient was still in intensive care unit, but its presence was overlooked at that time. The guidewire was retrieved completely during a surgery.

Atrial fibrillation induced by mad honey intoxication in a patient with Wolf–Parkinson–White syndrome

Grayanotoxins, which are extracted by bees from the leaves and fl owers of Rhododendron species, are the main compounds responsible for poisoning with honey in the Black Sea region. 1 “ Mad honey ” intoxication is usually a benign condition and is rarely fatal. In cases of toxication, bradycardia, atrioventricular (AV) block, and hypotension are commonly seen. Adequate fl uid replacement and 0.5 – 1.0 mg of atropine are suffi cient to improve the symptoms. We wish to report a case of a patient with Wolf – Parkinson – White syndrome (WPWS), who was admitted to hospital because of atrial fi brillation (AF) after “ mad honey ” ingestion. A 46-year-old man was admitted to the emergency department with dizziness and palpitations after eating a few spoonfuls of honey. He had no history of heart disease or drug usage. His blood pressure was 90/60 mmHg and his pulse rate was 172 beats per minute. A 12-lead electrocardiogram (ECG) demonstrated an irregular, wide QRS complex tachycardia (Fig. 1, top). Vital signs improved rapidly after saline infusion and sinus rhythm was restored within the following 20 – 30 min. A repeated ECG demonstrated a normal sinus rhythm, shortened PR intervals, delta waves, and minimally widened QRS complexes as WPWS (Fig. 1, bottom). All routine biochemical tests and thyroid functions were normal. Both his left atrial size and function were normal, as were his left ventricular size and function. He was monitored for 48 h, and AF did not recur. The patient was discharged with no medical therapy and transferred to an electrophysiology study for radio frequency ablation of the accessory bypass tract. Several cases of honey poisoning with bradyarrhythmia, sinus bradycardia, nodal rhythm, second-degree, or complete AV block were documented in recent literature; however, honey poisoning related to AF with WPWS has not previously been reported. 2 – 4

Clopidogrel-induced spontaneous pectoral hematoma.

Clopidogrel is an oral antiplatelet agent used in the treatment of coronary artery disease, peripheral vascular disease and cerebrovascular disease. Gastrointestinal symptomsincluding nausea, diarrhea and constipation are the common side effects ofthis drug. Serious side effects like intracranial hemorrhage and severe neutropenia were also reported but spontaneous pectoral hematoma due to the clopidogrel has not been reported previously. We present a case of large spontaneous pectoral hematoma during clopidogrel therapy in an elderly woman.

ECG Changes Due to Hypothermia Developed After Drowning: Case Report

SUMMARY Drowning is one of the fatal accidents frequently encountered during the summer and is the most common cause of accidental death in the world. Anoxia, hypothermia, and metabolic acidosis are mainly responsible for morbidty. Cardiovascular effects may occur secondary to hypoxia and hypothermia. Atrial fibrillation, sinus dysrhythmias (rarely requiring treatment), and, in serious cases, ventricular fibrillation or asystole may develop, showing as rhythm problems on electrocardiogram and Osborn wave can be seen, especially during hypothermia. A 16-year-old male patient who was admitted to our hospitals emergency service with drowning is presented in this article. In our case, ventricular fibrillation and giant J wave (Osborn wave) associated with hypothermia developed after drowning was seen. We present this case as a reminder of ECG changes due to hypothermia that develop after drowning. Response to cardiopulmonary resuscitation after drowning and hypothermia is not very good. Mortality is very high, so early resuscitation and aggressive treatment of cardiovascular and respiratory problems are important for life.

Acute coronary syndrome due to diclofenac potassium induced anaphylaxis: two Kounis syndrome variants in the same patient.

Hypersensitivity reactions associated with underlying coronary artery disease (Kounis syndrome) are not rare, despite the fact that they are not frequently documented in the medical literature especially if induced by diclofenac potassium (DP) (1-3). We present a patient with ST-segment changes who suffered an anaphylactic reaction after oral administration of DP. A 74-year-old woman was referred to our emergency department approximately 30 minutes after taking oral DP. On admission, the patient was complaining of retrosternal chest pain and generalized erythema. She had no history of allergy. Her blood pressure was 60/35 mmHg. After the first evaluation, intravenous antihistaminic and 40 mg of prednisolone, saline and dopamine infusions at rate 10 mg/kg/minute over 1 hour were administered. Her electrocardiogram (ECG) recording showed 1 mm ST-elevation in inferior derivations and third degree atrioventricular (AV) block (Fig. 1a). On admission to coronary care unit (CCU), the patient was hemodynamically stable, her cardiovascular examination was normal. Serial electrocardiographic recordings showed regression of ST-segment elevations and recovering AV block. (Fig. 1b). Cardiac enzymes were normal but serum IgE level (197 IU/mL) showed significant elevation (normal ranges 20-100 IU/mL). After stabilization, coronary angiography demonstrated two sequential 70% right coronary artery lesions and a non-critical lesion in the left anterior descending artery (Fig. 2). She underwent successful coronary angioplasty with implantation of sequential 3.0x16 mm and 3.0x8 mm bare-metal stents. Two months later, the patient was admitted to our hospital complaining of upper respiratory tract infection symptoms. After first evaluation (the patient and relatives did not warn the physician about drug allergy) intravenous DP was administered. The patient had felt chest pain and the ECG showed the same findings as observed during her previous application (Fig. 3). After intravenous antihistaminic and prednisolone administrations, the patient was hemodynamically stabilized and serial ECG recordings showed regression of STelevations. Dipyridamole myocardial perfusion scintigraphy showed no ischemic tissue of myocardium. Kounis Syndrome also known as “the allergic angina syndrome” has two variants. Type I variant includes patients with normal coronary arteries and Type II variant includes patients with culprit but quiescent pre-existing atheromatous disease where the acute release of inflammatory mediators can induce coronary artery spasm with normal or elevated cardiac enzymes and troponins (3-5). In our case, we observed STsegment elevations in inferior derivations due to coronary artery spasm with underlying coronary artery disease. For this reason, we think that our case could be an example for type II Kounis syndrome at first application. However, the same electrocardiographic and clinical findings were observed after the next administration of intravenous DP. We did not perform again coronary angiography because myocardial perfusion imaging showed no coronary ischemia. Our case is an example for both types I at the second application because of no coronary ischemia after coronary stenting and type II Kounis syndrome at the same time. These two events showed that the main mechanism is coronary spasm with or without coronary lesions.

The Effect of Admission Creatinine Levels on One-Year Mortality in Acute Myocardial Infarction

Background. We have known that patients with renal insufficiency (creatinine level) have increased mortality for coronary artery disease. In this study, the relationship between admission creatinine level and one year mortality are evaluated in patients with acute myocardial infarction (AMI). Method. 160 AMI patients (127 men and 33 women with a mean age of 59 ± 13) were enrolled in the study. Serum creatinine levels were measured within 12 hours of AMI. The patients were divided into two groups according to admission serum creatinine level. (1) elevated group (serum creatinine > 1.3 mg/dL) and (2) normal group (≤1.3 mg/dL). One year mortality rates were evaluated. Results. Elevated serum creatinine is observed in the 27 patients (16.9%). The mean creatinine level is 1.78 ± 7 mg/dL in the elevated group and 0.9 ± 0.18 mg/dL in the normal group (P < 0.0001). The mortality rate of the elevated group (n = 7, 25.9%) is higher than that of the normal group (n = 9, 6.8%). A significant increase in one year mortality is also observed (P=002) 60. Conclusion. The mildly elevated admission serum creatinine levels are markedly increased to one year mortality in patients with AMI.

Two Cases of Multivessel Coronary Artery Ectasias Resulting in Acute Inferior Myocardial Infarction

The incidence of multivessel coronary artery ectasias (CAEs) among patients undergoing coronary artery angiography is very rare. All three coronary vessels can be affected by CAE, but most patients have an isolated arterial ectasia, commonly the right coronary artery. In this report we present two cases with inferior myocardial infarction that was likely caused by thrombotic occlusion of CAEs.

Cutaneous analgesia before transradial access for coronary intervention to prevent radial artery spasm

Aim: Transradial access (TRA) for coronary intervention is increasingly used in current clinical practice. The aim of the present study was to evaluate the hypothesis that cutaneous analgesia before TRA for coronary intervention at a puncture site 30 minutes before puncture can reduce patient discomfort and the incidence of radial artery spasm (RAS). Methods: Patients (n=104) undergoing planned coronary interventions using TRA were prospectively randomized to receive either 1 mL of 1% lidocaine subcutaneously (n=52) (control group) or subcutaneous lidocaine plus 5% lidocaine cream (n=52) cutaneously 30 minutes before puncture (treatment group). The primary endpoint was angiographically or clinically confirmed RAS. Secondary endpoints were the occurrence of patient discomfort in the forearm during the procedure and access-site crossover to the femoral artery. Patient discomfort was quantified with a visual analogue scale (VAS) score. Results: Fifty-two patients in the treatment group (60.5±9.4 years of age and 16 female) and 52 patients in the control group (60.4±9.7 years of age and 16 female) were included in the final analysis. Radial artery spasm occurrence decreased in the treatment group compared to the control group (26.9% vs 9.6%; p=0.04) accompanied by a VAS score of 3.7±1.8 in the treatment group and 4.9±2.0 in the control group; p=0.02. The access site crossover rate did not differ between the groups (7.6% vs 21.1%; p=0.09). Conclusion: Cutaneous analgesia before TRA for coronary interventions is associated with a substantial reduction in the RAS and the procedure-related level of patient discomfort.