Huseyin Gunduz

Cardiac emergencies caused by honey ingestion: a single centre experience

An unusual type of food poisoning is commonly seen in the Black Sea coast of Turkey attributable to andromedotoxin containing toxic honey ingestion. This study is a retrospective case series of 19 patients admitted to an emergency department in 2002, poisoned by “mad” honey. All of the patients had the complaints of nausea, vomiting, sweating, dizziness, and weakness, several hours after ingesting “mad” honey. Physical examination showed hypotension in 15 patients, sinus bradycardia in 15, and complete atrioventricular block (AVB) in four patients on admission. Two patients with bradycardia and two with AVB fell and injured their heads. Three of them presented with local haematoma. One patient had a 6 cm cut on his head without any neurological deficit and his cranial computed tomography imaging was normal. Hypotension and conduction disorders resolved with atropine treatment, resulting in complete recovery within 24 hours.

Myocardial bridging as a cause of acute myocardial infarction: a case report

BackgroundSystolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation.Case presentationA 33 year-old-man was admitted to our emergency with acute anteroseptal myocardial infarction after a blood donation. The electrocardiography showed sinus rhythm and was consistent with an acute anteroseptal myocardial infarction. We decided to perform primary percutanous intervention (PCI). Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery on coronary angiogram. PCI was canceled and medical follow up was decided. Blood transfusion was made because he had a deep anemia. A normal hemaglobin level and clinical reperfusion was achieved after ten hours by blood transfusion. At the one year follow up visit, our patient was healthy and had no cardiac complaints.ConclusionsMyocardial bridging may cause acute myocardial infarction in various clinical conditions. Although the condition in this case caused profound anemia related acute myocardial infarction, its treatment and management was unusual.

Isolated Interrupted Aortic Arch: A Case Report and Review of the Literature

An 18-years-old male presented to emergency department after a car accident with the diagnosis of femoral bone fracture. Arterial blood pressure was 160/90 mmHg in both arms. Bilateral femoral and popliteal pulses were extremely weak and there was systolic ejection murmur on the left second intercostals area. Chest X-ray showed rib notching with normal cardiac silhouette. Transthoracic echocardiography showed the aortic interruption just below the left subclavian artery. Aortography showed a complete interruption of the aortic arch (IAA) just distal to the origin of the left subclavian artery. Femoral bone fracture was treated by conservative strategy. A gadolinium contrast-enhanced magnetic resonance angiogram (1.5 T scanners) clearly reaffirmed a complete interruption of the descending aorta, 3.6 cm from the left subclavian artery with extensive collateralizations. Mild degree hypertension was controlled by a long acting calcium channel blocker. Later the patient has been scheduled for elective surgical repair. We aimed to discuss the diagnostic and treatment options of the interrupted aortic arch as being a rare anomaly.

In vivo effect of losartan on platelet aggregation in patients with hypertension

The angiotensin II receptor, losartan, has been found to inhibit platelet aggregability to some extent in in vitro experiments. There have been conflicting results about the in vivo effects of losartan. We sought to clarify the in vivo effect of losartan on platelet aggregation. Forty patients with grade I essential hypertension were treated with losartan for 3 weeks. Platelet aggregation tests with adenosine diphosphate (ADP) and ristocetin were analyzed and compared before and at the end of the study. Losartan effectively decreased systolic (SBP) and diastolic (DBP) blood pressure. Mean SBP before and after treatment was 159.6 ± 12.8 and 149.2 ± 17.3u2009mmHg, respectively. Mean DBP decreased from 93.7 ± 8.2 to 87.7 ± 10.3u2009mmHg after treatment. The results of the platelet aggregation tests with ADP and ristocetin were not significantly different when both rate and amplitude of maximal aggregation were included. Peak platelet aggregation with ADP regarding the lowest light transmission in the aggregometer was 59.8% ± 24.3% before and 58.3% ± 18.1% after the treatment. The same variables with ristocetin were 66.8% ± 21.6% and 60.8% ± 23.3%, respectively. In vivo effects of losartan on platelet aggregation with ADP and ristocetin were insignificant.

A case of coronary artery fistula with mitral stenosis

Coronary artery fistulae, being a rare form of congenital anomalies of the coronary arteries, are usually discovered by chance during coronary arteriography. However, these fistulae can cause an important coronary morbidity and mortality leading to angina, syncope, congestive heart failure, myocardial infarction and sudden death. The coincidence of mitral stenosis and congenital artery fistula is rare in the literature. In our case report, a patient with a coronary artery fistula originating from the circumflex, draining to the main pulmonary artery, discovered at cardiac catheterization and coronary angiography done with a prediagnosis of mitral stenosis is presented in the light of the literature.

Does the prevalence of nasal polyps increase in patients using statins

Several statins inhibit T-helper 1 development and induce T-helper 2 polarization and production of T-helper 2 cytokines that promote the activation and chemotaxis of eosinophils. Whether statins promote the development of nasal polyps has so far been uncertain. No studies have evaluated the frequency of the development of nasal polyps in patients using statins. To better define the relationship of statin use to the presence of nasal polyps, the investigators explored the frequency of the development of nasal polyps in patients who were using statins. A total of 200 patients who were using statins and 200 who were not using statins (400 cases) were investigated. All patients were examined for nasal polyps by anterior rhinoscopy or investigation with a fiberoptic endoscope. In addition, immunoglobulin E levels were measured, a skin prick test was performed, and the results from the 2 groups were compared. Nasal polyps were detected in 4 subjects who were using statins, whereas 5 nasal polyps were found in the control group; differences between the 2 groups were statistically insignificant (P> .05). When the atopy status of the 2 groups was compared, prick test positivity and serum immunoglobulin E levels were found to be 15% and 44±31 IU/mL in the statin group and 19% and 68±23 IU/mL in the control group (P> .05). These results show that nasal polyposis is a multifactorial disease with several different causes; however, the frequency of the development of nasal polyps does not increase in patients who use statins.