Arrhythmias during and after zoledronic acid infusion patients with bone metastasis.

Zoledronic acid (ZA) is one of the important bisphosphonates which is widely used in bone metastatic cancer and osteoporotic patients. In a few studies, it has been reported that treatment with bisphosphonates was associated with an increased risk of atrial fibrillation. We aimed to evaluate the arrhythmias that developed during and immediately after infusion of the ZA. Fifty-two bone metastatic patients were included in the study group. All patients had 24-h Holter monitorization during the first dose ZA infusion day. All of the patients had 4-h basal cardiac rhythm records before ZA infusion and about 19 h after infusion. A short survey including demographic data and past medical history has been completed. None of patients had clinically important arrhythmias before ZA infusion. We divided arrhythmias into two groups as supraventricular and ventricular. We evaluated arrhythmias in pre-infusion, during infusion, and post-infusion periods. ZA was administered 4 mg intravenously (IV) in 15 min. Thirty-three of patients (63.5 %) were male and 19 (36.5 %) patients were female. Mean age of the patients was 53.9 ± 11.8 years. Most frequent cancers were breast (25 %) and lung cancer (15.3 %). Twelve (23 %) patients had history of mediastinal radiotherapy. In basal records, we detected that twenty-four (46 %) of patients had supraventricular premature complexes (SVPC) or ventricular premature complexes (VPC). Fifteen (28.8 %) of patients had SVPC and fourteen (26.9 %) had VPC during infusion period. After infusion period, 48 (92.3 %) of patients had SVPC and 41 (78.8 %) had VPC. Only 3 patients had no arrhythmia after infusion. Three patients had sinus arrhythmia and two had Mobitz type 2 atrioventricular blocks after infusion. One patient, who had no history of comorbidities and had SVPC in the basal records, developed atrial fibrillation that was refractory to medical cardioversion after 10 days of seventh dose of ZA infusion. In this study, we found that both SVPC and VPC increased in cancer patients treated with ZA. Furthermore, ZA may induce clinically important arrhythmias.

Zolmitriptan-induced acute myocardial infarction.

Triptans are an established treatment for acute migraine attacks. By activating 5HT1B/1D receptors they lead to vasoconstriction of the cerebral blood vessels which are dilated during migraine attacks. Moreover, they reduce secretion of vasoactive peptides and conduction of pain stimuli over the cerebral cortex. In up to 7% of cases of treatment with triptans, thoracic pain occurs, although this is mostly transient, mild and without lasting ischemia. We present the case of a 45 year-old woman with a history of migraine with visual aura since the age of 20. She had no history of diabetes mellitus, hypertension, smoking or any other risk factors for cardiovascular events before she was admitted to our emergency room with typical chest pain. An electrocardiogram revealed anterior myocardial infarction following her monthly dose of oral zolmitriptan. Catherization revealed a normal coronary arterial system. The laboratory indices for cardiac risk were within normal ranges. The patient was advised to avoid triptans permanently on being discharged.

A case of systemic lupus erythematosus presenting with hypereosinophilia and Loeffler endocarditis.

A 15-year-old boy who was admitted to the neurology department had multiple cerebral infarcts on cranial magnetic resonance imaging. A transthoracic echocardiogram revealed myocardial thickening and apical thrombus in the left ventricle suggesting Loeffler endocarditis. There was remarkable hypereosinophilia on the haemogram. An investigation for the aetiology of hypereosinophilia led to the diagnosis of systemic lupus erythematosus and associated antiphospholipid syndrome. This case represents a very rare case of systemic lupus erythematosus in which the initial presentation was hypereosinophilia related Loeffler endocarditis.

[Thrombosed giant proximal pulmonary artery aneurysm]. / Trombozlu dev proksimal pulmoner arter anevrizmasi.

We present a 36-year-old male patient with a previous diagnosis (22 years) of Eisenmenger's syndrome, who had a giant proximal pulmonary artery aneurysm complicated by massive thrombus formation. The patient experienced paroxysmal atrial fibrillation attacks for the past month. His functional capacity was New York Heart Association class III. Chest radiography showed aneurysmal dilatation in the left pulmonary artery. The patient was assessed by transthoracic echocardiography and multislice computed tomography. There was mild narrowing in the thick and calcified pulmonary valve (peak systolic gradient 35 mmHg) and moderate regurgitation. The mean pulmonary artery pressure was estimated as 50 mmHg. The diameters of the main, left, and right pulmonary arteries were 6.5 cm, 10 cm, and 3.7 cm, respectively. There was a massive thrombus in the aneurysmatic left pulmonary artery. The patient was referred to the cardiovascular surgery department for pulmonary artery reconstruction and cardiopulmonary transplantation. In addition, medical treatment was instituted with warfarin for thrombus and paroxysmal atrial fibrillation, metoprolol for atrial fibrillation, and bosentan for pulmonary hypertension. The patient's functional capacity showed improvement after the first month of medical treatment and no complications were seen within a year follow-up.

Two cases of endomyocardial disease with hypereosinophilia in Turkey.

Endomyocardial disease is characterized by fibrothrombotic thickening of apical endocardium and subvalvular regions of atrioventricular valves. The disease is uncommon in Turkey. In this report two cases of endomyocardial disease with hypereosinophilia which were medically managed are presented.

Increased levels of high sensitive C-reactive protein in patients with chronic rheumatic valve disease: evidence of ongoing inflammation.

The precise pathogenetic mechanism(s) of rheumatic fever and rheumatic heart disease have never been defined. C-reactive protein (CRP) is increased in patients with acute rheumatic fever, but it is not known whether plasma levels increase in patients with chronic rheumatic valve disease. The aim of this study was to determine the role of inflammation detected by high sensitivity CRP (hs-CRP) levels in the progression of chronic rheumatic valve disease. A total of 113 patients with chronic rheumatic valve disease (81 women, 32 men; mean age 40+/-14 years, range 13-70), 51 patients with prosthetic valve(s) (31 women, 20 men; mean age 48+/-13 years, range 21-71) and 102 healthy subjects (68 women, 34 men, mean age 41+/-12 years, range 25-73), as a control group, were assessed. Patients with acute rheumatic fever, acute infection, inflammatory disease, malignancy, acute myocardial infarction and trauma were excluded. hs-CRP was determined using latex-enhanced immunonephelometric assays on a BN II analyzer (Behring). Transthoracic echocardiography was performed in all patients in order to evaluate valvular disease. Levels of hs-CRP were significantly higher in patients with chronic rheumatic heart disease than in patients with prosthetic valve(s) and healthy subjects (0.62+/-0.64 vs. 0.35+/-0.41 vs. 0.24+/-0.18 mg/l, P<0.01 and P<0.001 respectively). No correlation was observed between CRP and age, sex or functional capacity. We found that hs-CRP is increased in chronic rheumatic heart disease; this may indicate that inflammatory response still persists in the chronic phase.