Simultaneous occurrence of a large asymptomatic prolapsing left atrial myxoma with a cutaneous squamous cell carcinoma.

Synchronous myxoma of the heart and other malignancies are extremely rare. We report a case of a 64-year-old man who had a large left atrial myxoma that obstructed the mitral valve, as well as an unrelated, coexistent cutaneous squamous cell carcinoma in the sacral area. During the preoperative evaluation for non-cardiac surgery, the tumor was diagnosed coincidentally by echocardiographic examination. Echocardiography findings were consistent with a large left atrial myxoma originating from the posterior wall and prolapsing into the left ventricular cavity through the mitral valve, causing mitral stenosis. The mass was successfully completely excised. Histologic examination of the mass confirmed the diagnosis of cardiac myxoma. We report a casual echocardiographic finding of a left atrial myxoma that obstructed the mitral valve outflow tract, and an unrelated, synchronous cutaneous squamous cell carcinoma in the sacral area.

Apolipoprotein E genotype in patients with cerebrovascular diseases and its effect on the disease outcome.

A total of 100 hospitalized stroke patients and 30 healthy controls were included in a study aiming to determine the predictive role of ApoE genotype polymorphism for stroke outcome in the Turkish population. The most frequent ApoE genotype was epsilon3/3 reflecting Asian population polymorphic distribution. ApoE polymorphism in the Eastern Turkish population was found to be independent of stroke type, OSCP subtypes of infarction, localization of hemorrhage, severity of carotid artery stenosis, and resultant stroke outcome. Distinct polymorphic results in populations from nearby regions suggest a multifactorial pathogenesis and presence of very complex genetic factors in the development of stroke and stroke outcome.

Spontaneous coronary artery dissection during hemodialysis in the post-abortion period.

Spontaneous coronary dissection (SCAD) is an unusual cause of acute myocardial infarction with complex pathophysiology. We present a case of acute inferior myocardial infarction resulting from spontaneous coronary artery dissection of the right coronary artery in a 33-year-old woman during the hemodialysis due to a recent abortion and consequent curettage at first trimester of her pregnancy. This report describes a previously healthy woman without traditional cardiovascular risk factors who presented with an acute inferior myocardial infarction. Spontaneous coronary artery dissection (SCAD) should be considered as a cause of the acute myocardial infarction in young patients without traditional risk factors for coronary artery disease, in females in the both peri-partum and post-abortion period.

Pulmonary hypertension in patients with essential thrombocythemia and reactive thrombocytosis.

Increased incidence of pulmonary hypertension (PH) has been reported in patients with chronic myeloproliferative disorders. The exact incidence of PH in essential thrombocythemia (ET) is unknown. Most of the reported literature consists of case reports or small studies. We designed this study to asses the incidence of PH in patients with ET and reactive thrombocytosis. Previously or newly diagnosed 46 patients with ET, and 40 patients with reactive thrombocytosis secondary to iron deficiency anemia were found to be eligible for this study. Diagnosis of PH was established via transthoracic echocardiography. PH was found in 22 (47.8%) out of 46 patients with ET. Seven patients with PH were newly diagnosed ET, 5 patients with PH were in low, and the other patients with PH were in intermediate or high risk category. We found statistically significant difference in terms of platelet counts between ET patients with PH and without PH (p = 0.027). None of the patients with reactive thrombocytosis had PH. In conclusion, PH appears to be common in patients with ET. Therefore, all patients with ET should be evaluated for PH. Larger and prospective studies are required to clarify the long-term impact of PH on the survival of these patients. Future studies are also needed to determine whether cytoreductive treatment and aspirin prevent the development of PH, and to determine the effects of cytoreductive treatments and aspirin on the prognosis of PH. The effect of PH on ET prognosis should also be determined in low risk ET patients.

Coexisting subarachnoid hemorrhage and subdural hematoma mimicking acute anterolateral myocardial infarction.

Ischemic electrocardiographic changes, elevations in cardiac-specific markers such as troponin and creatinine phosphokinase MB, segmental wall motion abnormalities, and myocardial dysfunction may occur after central nervous system events such as subarachnoid hemorrhage, subdural hematoma, and ischemic stroke. The pathophysiology remains unclear, but a catecholamine-induced neurocardiogenic injury has been mentioned as a causative factor. We reported a case of coexisting subarachnoid hemorrhage and subdural hematoma with ischemic electrocardiography changes, increases in cardiac-specific enzymes, and a regional wall motion abnormality despite normal epicardial coronary arteries. It is very important to differentiate neurogenic stunned myocardium from myocardial dysfunction caused by coronary artery disease in patients with intracranial hemorrhages for appropriately managing the treatment of cases.

Elevated plasma N-terminal pro-brain natriuretic peptide levels in acute ischemic stroke.

BACKGROUND: B-type natriuretic peptide (BNP) is a neurohormone secreted mainly in the cardiac ventricles in response to volume expansion and pressure overload. The aim of this study was to assess plasma N-terminal proBNP (NT-proBNP) changes in acute ischemic stroke (AIS). METHODS: The study group consisted of 57 (37 women aged 64 +/- 12 years) patients who had their first AIS and no history or signs of cardiovascular disease. An age-matched control group was also included (n = 57, 36 women aged 61 +/- 6 years). NT-proBNP, troponin I (TnI), and creatine kinase-MB were evaluated. A thorough cardiovascular and neurological investigation, including imaging techniques and lesion size determination, was also performed. RESULTS: The log NT-proBNP peak levels, TnI, and creatine kinase-MB levels were significantly higher in AIS compared with controls (7.25 +/- 1.77 vs 3.48 +/- 0.76 pg/mL, P < .0001; 0.76 +/- 0.54 vs 0.5 +/- 0.0 ng/mL, P < .001; 57 +/- 37 vs 13 +/- 4 U/L, P < .001, respectively). The log NT-proBNP correlated positively with TnI (r = 0.29, P = .03) and heart rate (r = 0.41, P = .002), and negatively with left ventricular ejection fraction (r = -0.67, P < .0001). Patients with signs of marked myocardial ischemia and patients with insular cortex involvement had even higher NT-proBNP levels. After adjustment for relevant factors, the relation between the log NT-proBNP and AIS as well as insular cortex involvement was observed to be insignificant (P > .05 for both). CONCLUSIONS: Our results show that NT-proBNP plasma levels are significantly elevated in AIS and might be of clinical importance as a supplementary tool for the assessment of cardiovascular function in patients with AIS.

Hepatopulmonary syndrome and right ventricular diastolic functions: an echocardiographic examination.

AIM: Liver functions are affected in the course of cardiac diseases, and similarly, liver diseases affect cardiac functions. Many studies in the literature have shown that left ventricular systolic and/or diastolic dysfunction may develop during chronic liver disease. However, there are limited studies investigating right ventricular functions during chronic liver diseases. METHODS: A total of 84 patients who had no systolic and/or diastolic dysfunction in the left ventricle (LV) were evaluated; 46 patients with liver cirrhosis; 10 (21.74%) cirrhotic patients with hepatopulmonary syndrome (HPS) (group 1), 36 (78.26) cirrhotic patients without HPS (group 2), and 38 healthy individuals were treated as control. RESULTS: Right ventricular diastolic dysfunction was determined in all patients of group 1 (100%), 26 of group 2 (72.22 %), and 4 of the controls (10.52%) (P<0.05). Tricuspid deceleration time (dt) was significantly different between the groups (P<0.05). In addition, right atrium (RA) diameters, right ventricle (RV) diameters, and RV wall thickness were significantly different between the groups (P<0.05). Pulmonary artery pressure (P<0.05) and pulmonary vascular resistance (P<0.05) were also seen to be higher in group 1 than those in group 2 and control group. CONCLUSIONS: Right ventricular diastolic dysfunction rate is high in chronic liver diseases. In the presence of HPS, right ventricular diastolic dysfunction is more remarkable in patients than those without HPS. Right ventricular diastolic dysfunction may result in dilatation and hypertrophy in the right heart.

N-terminal proBNP plasma levels correlate with severity of mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: Brain natriuretic peptide (BNP), a neurohormone, is secreted predominantly from the ventricular myocardium. Studies investigating BNP secretion in diseases affecting the right side of the heart are scarce. The relationship between N-terminal proBNP (NT-proBNP) and echocardiographic and clinical findings was studied in cases with isolated moderate to severe rheumatic mitral stenosis (MS), and in patients with previous mitral valve replacement (MVR). METHODS: Thirty-two patients with MS (mean age 41.2 +/- 5.7 years), 20 with MVR (mean age 46.0 +/- 4.6 years) and 30 healthy individuals (mean age 40.3 +/- 4.9 years) were included in the study. In addition to NT-proBNP measurements, detailed transthoracic echocardiography was performed in all patients and healthy subjects. RESULTS: Plasma levels of NT-proBNP were significantly higher in patients with MS than in those with MVR or in controls (99.8 +/- 12.7 versus 74.7 +/- 6.9 and 48.5 +/- 10.5 pg/ml, respectively; p <0.0001 all groups). NT-proBNP levels showed a significantly greater increase in severe MS than in moderate MS (109.8 +/- 5.6 versus 88.3 +/- 7.6 pg/ml, p <0.0001). NT-proBNP levels also were higher in MVR patients than in controls (74.7 +/- 6.9 versus 48.5 +/- 10.5 pg/ml; p <0.0001). Although NT-proBNP levels did not correlate with left ventricular ejection fraction (LVEF) in patients with MS (r = -0.33; p >0.05), there was a positive correlation with pulmonary artery pressure (r = 0.87; p <0.001) and a negative correlation with mitral valve area (MVA) (r = -0.89; p <0.0001). However, multivariate analysis identified only MVA as an independent correlate of NT-proBNP (beta = -0.47; p = 0.02). CONCLUSION: In patients with rheumatic MS, NT-proBNP levels correlated positively with MS severity. Moreover, NT-proBNP levels increased significantly in patients with MS, but were significantly lower in those who underwent MVR.

Insulin response to oral glucose loading and coronary artery disease in nondiabetics.

Hyperinsulinemia is related to coronary artery disease (CAD), as an indication of decreased insulin sensitivity. Although there are many studies showing the relation between fasting insulin levels and insulin resistance, there are fewer studies on postprandial insulin levels. The aim of the present study was to investigate the relationship between postprandial insulin levels and CAD and its extent in our patients. For this purpose, oral glucose tolerance testing was performed in 222 patients with no known diabetes and who were scheduled to undergo diagnostic coronary angiography. The patients were first separated into two groups, one group (group I) having an insulin response within reference values to oral glucose loading, and the other group (group II) with a higher than normal insulin response. The presence and extent of CAD in the two groups were compared. While 65% of the patients in group 1 had CAD, this rate increased to 79% in group 2 patients (P = 0.02). The mean vessel scores were 0.92 +/- 0.78 in group 1 and 1.67 +/- 0.99 (P < 0.0001) in group 2 patients. The stenosis scores were 2.192 +/- 2.077 in group 1 and 5.588 +/- 3.519 (P < 0.001) in group 2, while the extent scores were 1.230 +/- 1.292 in group 1 and 2.729 +/- 1.847 in group 2 (P < 0.0001). The differences between the two groups were significant. Postprandial insulin values were positively correlated with CAD (P = 0.001, r = 0.214), vessel scores (P < 0.0001, r = 0.326), stenosis scores (P < 0.0001, r = 0.261), and extent scores (P < 0.0001, r = 0.419). Logistic regression analysis revealed hyperinsulinemia increased CAD independent from the other risk factors (OR = 5.742, CI 95%: 1.809-18.227, P = 0.003).

Iatrogenic left atrioventricular fistula after aortic valve re-replacement.

Left ventriculoatrial fistula is a very rare cardiac disorder. The case is reported of a male patient who was admitted to the authors' clinic with dyspnea and fatigue. The patient had an atrioventricular fistula between the left atrium and left ventricle, and had undergone aortic valve re-replacement for prosthesis malfunction about one year previously. The fistula was considered to be the result of iatrogenic injury related to valve re-replacement surgery.

Clinical investigation: thyroid function test abnormalities in cardiac arrest associated with acute coronary syndrome.

INTRODUCTION: It is known that thyroid homeostasis is altered during the acute phase of cardiac arrest. However, it is not clear under what conditions, how and for how long these alterations occur. In the present study we examined thyroid function tests (TFTs) in the acute phase of cardiac arrest caused by acute coronary syndrome (ACS) and at the end of the first 2 months after the event. METHOD: Fifty patients with cardiac arrest induced by ACS and 31 patients with acute myocardial infarction (AMI) who did not require cardioversion or cardiopulmonary resuscitation were enrolled in the study, as were 40 healthy volunteers. The patients were divided into three groups based on duration of cardiac arrest (<5 min, 5-10 min and >10 min). Blood samples were collected for thyroid-stimulating hormone (TSH), tri-iodothyronine (T3), free T3, thyroxine (T4), free T4, troponin-I and creatine kinase-MB measurements. The blood samples for TFTs were taken at 72 hours and at 2 months after the acute event in the cardiac arrest and AMI groups, but only once in the control group. RESULTS: The T3 and free T3 levels at 72 hours in the cardiac arrest group were significantly lower than in both the AMI and control groups (P < 0.0001). On the other hand, there were no significant differences between T4, free T4 and TSH levels between the three groups (P > 0.05). At the 2-month evaluation, a dramatic improvement was observed in T3 and free T3 levels in the cardiac arrest group (P < 0.0001). In those patients whose cardiac arrest duration was in excess of 10 min, levels of T3, free T3, T4 and TSH were significantly lower than those in patients whose cardiac arrest duration was under 5 min (P < 0.001, P < 0.001, P < 0.005 and P < 0.05, respectively). CONCLUSION: TFTs are significantly altered in cardiac arrest induced by ACS. Changes in TFTs are even more pronounced in patients with longer periods of resuscitation. The changes in the surviving patients were characterized by euthyroid sick syndrome, and this improved by 2 months in those patients who did not progress into a vegetative state.

Recurrent multiple cardiac hydatidosis.

Cardiac hydatid cyst is an uncommon disease. We report on a woman admitted to our clinic with chest pain and palpitations. The ECG showed anterior ischemia, and coronary anatomy was normal. The diagnosis was: multiple cardiac hydatid cysts, for which she had undergone surgery 4 years earlier for a 5 x 5 hydatid cyst and treated with albendazole. Despite this, there was a recurrence of multiple cysts. Recurrence of intracavitary hydatid cyst is rare, and surgical treatment of multiple, small cysts remains controversial.

Assessment of acute phase proteins in acute ischemic stroke.

Acute phase proteins (APPs) have been implicated to play important roles during both acute and chronic inflammatory processes in different diseases including ischemic stroke. Though there are several studies showing the importance of APPs as inflammation markers in acute ischemic stroke (AIS), the time course of these proteins during acute phase of AIS is not well known. Thus, the aim of this study was to show the changes in plasma levels of six APPs (i.e., haptoglobin [Hp], ceruloplasmin [Cp], high-sensitive C-reactive protein [h-CRP], fibrinogen, complement 3 [C3] and complement 4 [C4]) during the first 10 days after acute stroke. The study group consisted of 34 female and 19 male patients (n = 53; mean age 65 +/- 12 years), who had first acute ischemic stroke (AIS). An age-matched control group (n = 53; 32 female and 21 male subjects, mean age 62 +/- 6 years) was also included. To evaluate the plasma levels of six APPs, the blood samples of patients with AIS were withdrawn on admission (day 1), and after 3, 5 and 10 days, whereas only one measurement was performed in the control group. In addition, several cerebrovascular risk factors were determined. The peak levels of APPs were higher in the AIS group than the control group (p < 0.0001). In serial measurements, the levels of h-CRP, Hp, C3 and C4 showed alterations during 10 days after AIS (p < 0.0001, p < 0.05, p < 0.0001, p < 0.0001, respectively). The alterations in levels of fibrinogen and Cp were not statistically significant (p > 0.05). After stroke, h-CRP, C3 and fibrinogen reached their highest values on the third day, Cp and C4 on the fifth day, and Hp on the tenth day. The plasma levels of h-CRP correlated positively with other five APPs studied (p < 0.05). These findings support the importance of inflammation processes after stroke. We suggest that the differences in levels of APPs could be used in predicting the outcome of stroke patients.

Complement activation in acute coronary syndromes.

The complement system is part of the host defence response. However, considerable evidence suggests that complement plays an important role in the pathophysiology of ischemic heart disease. The aim of this study was to evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury. The study population included 152 subjects (26 females): 82 with ACS (35 acute myocardial infarction (AMI), 22 non-Q wave MI (NQMI), 25 unstable angina (UAP)) (Group A), 35 stable angina (SA) (Group B), and 35 healty control subjects (Group C). Complement 3 (C3), Complement 4 (C4), C-reactive protein (CRP), troponin I (TnI) as well as creatine kinase MB (CK-MB) were evaluated. Patients' blood samples were taken on admission (day 1) and after 2, 3 and 7 days in group A. However, only one measurement was performed in the groups B and C. Plasma C3 and C4 peak levels were significantly higher in patients with AMI (141+/-29 and 35+/-11 mg/dl) and NQMI (136+/-13 and 35+/-7 mg/dl) than in patients with SA (128+/-14 and 27+/-10 mg/dl) and the control subjects (114+/-22 and 22+/-7 mg/dl) (p<0.03). Also, C3 and C4 serum levels in patients with SA and UAP (126+/-16 and 31+/-7 mg/dl) were significantly higher than those in control subjects (p<0.01, p<0.03, respectively). At 1-week follow-up, there were no significant differences between the plasma levels of C3 and C4 in patients with UAP (p>0.05). However, plasma levels of C3 and C4 were significantly different between days in patients with AMI and NQMI (p<0.0001). Plasma C3 and C4 levels in ACS showed a relationship with peak CK-MB and Tn I levels (p<0.01). Plasma CRP level in ACS showed positive correlation with C3 (p<0.01) and C4 (p<0.001). In this study, we determined that plasma C3 and C4 levels were elevated in ACS and SA. Although C3 and C4 were higher in ACS and SA, the systemic levels of inflammatory markers in patients with SA and UAP were lower than those found in the AMI and NQMI groups. The relationship between C3, C4 levels and ACS further suggests that the complement activation is related to necrosis within the myocardium.

Serum cardiac troponin T levels as an indicator of myocardial injury in ischemic and hemorrhagic stroke patients.

Many studies in the literature have clearly shown the increase in creatine kinase-myocardial subfraction (CK-MB) levels and changes in electrocardiography (ECG) after stroke. However, the studies on cardiac troponin T (cTnT) which is more sensitive and specific to myocardium after stroke are relatively scarce. Moreover, its associations with volume of stroke lesions and type of stroke have not been investigated thoroughly. Thus, the aims of this study were to investigate a predictive value of cTnT in assessing myocardial injury and cardiac dysfunction in different types of stroke (hemorrhagic or ischemic stroke) and its relationship with stroke size and volume. This study included 62 patients (30 males and 32 females) with acute stroke confirmed by computed tomography (CT). Blood samples were obtained within 24 hours of stroke onset to measure the serum levels of creatin kinase (CK), CK-MB, lactate dehydrogenate (LDH), and cTnT. ECG and echocardiography were performed to assess myocardial function and left ventricular ejection fraction (LVEF). Of all patients included in the study, 20 patients (32%) demonstrated elevations in cTnT, while 28 patients (45%) had increased CK-MB levels. Serum levels of cTnT were positively correlated with stroke volume (r = 0.65, p < 0.0001), while inversely correlated with LVEF (r = -0.53, p < 0001). Serum levels of both CK-MB and cTnT were higher in patients with hemorrhagic stroke than those with ischemic stroke but this difference was not significant (p > 0.05). As a conclusion, cTnT has a higher specificity and sensitivity in detecting myocardial injury after stroke of both ischemic and hemorrhagic origins. Measurement of the serum levels of cTnT is of clinical importance in evaluating myocardial injury and provides a useful aid in estimating the volume of stroke lesions.

The association between NT-proBNP levels, functional capacity and stage in patients with heart failure.

OBJECTIVE: Amino-terminal probrain natriuretic peptide (NT-proBNP), a biologically inactive derivative of BNP, is clinically more useful owing to its longer half-life, higher plasma concentrations, lesser variation among individuals, and higher in vitro stability. In this regard, NT-proBNP may be a better indicator of the severity of ventricular dysfunction. In this study, the association of NT-proBNP levels with functional capacity and stage of heart failure was explored in patients with CHF. Also, we particularly focused on the presence and significance of neurohormonal activation in the group of patients classified as stage-A according to ACC/AHA guidelines. METHODS AND RESULTS: 64 patients with CHF (31 men, 33 women; mean age 58.26 +/- 10.59 y) and 36 healthy controls (24 men, 12 women; mean age 57.47 +/- 10.83) were included in this study. The New York Heart Association (NYHA) classification system (I, II, III, IV) was used to define the functional capacity; and the stage of the heart failure was based on the ACC/AHA guidelines (A, B, C, D). Healthy female participants had higher NT-proBNP levels compared to their male counterparts (p < 0.001). Left ventricular ejection fraction (LVEF) did not correlate significantly with functional capacity and stage of the disease. CHF patients had higher NT-proBNP compared to controls (p < 0.001). There was a positive correlation between NT-proBNP and functional capacity in patients, and NT-proBNP increased significantly with each increasing class of the disease. Similarly, a positive correlation existed between the stage of heart failure and NT-proBNP levels, which increased significantly with increasing stages of the disease. Patients with NYHA I and stage A disease had higher NT-proBNP levels compared to controls (p = 0.04). CONCLUSIONS: The severity of CHF can be objectively assessed by measuring the circulating levels of NT-proBNP. Even in NYHA I and stage A disease, NT-proBNP levels are higher compared to controls (p = 0.04). NT-proBNP can provide objective information regarding the severity of the disease and also aid in treatment decisions in patients with CHF.