Recent reports indicate that inflammatory mechanisms play a crucial role in the pathogenesis of atherosclerosis and neointimal proliferation as well as coronary restenosis. To provide baseline data for further studies regarding stenting, restenosis and inflammatory response, we prospectively conducted a clinical study to investigate the time related response of plasma levels of immunoglobulin-E (IgE) and C-reactive protein (CRP) which are two different inflammatory markers mediated by different cytokines in stable patients who underwent elective coronary artery stenting. Thirteen consecutive stable patients who underwent coronary artery stenting were included in the study. Levels of IgE and CRP were determined pre- and poststent implantation on four consecutive days and at the end of the first as well as third month. Levels of these two markers were gradually elevated on postprocedure days while reaching peak values on the second and third days for IgE (initial 278 ± 335 IU/mL vs peak 350 ± 489 IU/mL, P = 0.01) and CRP (initial 0.5 ± 0 mg/dL vs peak 2.7 ± 3 mg/dL, P = 0.002), respectively. High levels gradually returned to baseline values determined at the end of the first and even third months after stent implantation implying an acute inflammatory reaction. Stent implantation seems not to cause any persistent and ongoing inflammatory response in the long term.
Plasma levels of C-reactive protein (CRP) and serum amyloid A protein (SAA), inflammatory markers, and soluble thrombomodulin (s-TM), a marker of endothelial damage, are thought to be related to coronary artery disease. However, the relationship between these inflammatory markers and endothelial injury in atherosclerotic coronary arteries is still unclear. Fifty-five patients who underwent coronary angiography were classified into 3 groups according to the severity of left coronary arterial atherosclerosis evaluated by the Gensini score (GS; normal: score = 0, n = 15; mild: 0 < score < 15, n = 29; severe: score ≥ 15, n = 11). Blood samples were obtained from the aortic root (Ao) and coronary sinus (CS) and plasma CRP and SAA levels were measured by latex turbidimetric immunoassays, and s-TM levels were determined by an enzyme-linked immunosorbent assay. The difference between marker concentrations in the Ao and CS of the coronary circulation was expressed as the coronary sino-arterial (CS-Ao) difference. The CS-Ao differences of s-TM and SAA were significantly higher in patients with severe atherosclerosis than in normal patients (P < 0.01), and showed weak but significant positive correlations with the GS (r = 0.34, P < 0.01 and r = 0.33, P < 0.05, respectively). The CS-Ao differences in CRP did not differ among the three groups, and did not correlate with the GS. The results of our study reveal a possible relationship between endothelial cell injury and inflammation in atherosclerotic coronary arteries.
There have been many studies investigating the association between gene polymorphisms and coronary artery disease (CAD) including myocardial infarction (MI), and some studies have shown that certain gene polymorphisms are associated with CAD/MI. However, the results of the association have sometimes been controversial. The reason may be that the contribution of genetic risk factors to CAD/MI varies depending on the ethnic, environmental, and habitual backgrounds, and differs between males and females. In this study, we analyzed 17 polymorphisms in 12 candidate genes for MI in 136 patients and 200 to 235 controls, and found that there is a significant association of MI with the polymorphisms in the genes for E-selectin and CD14 receptor. To further explore the association, we investigated the C-260 T polymorphism in the promoter region of the CD14 gene in 502 MI patients and 527 control subjects. The genotype distributions of the CD14 polymorphism were as follows; patients; T/T 32.5%, C/T 48.2%, C/C 19.3%, and controls; T/T 25.4%, C/T 52.8%, C/C 21.8%. The frequencies of the T/T homozygotes were significantly higher in the patients (OR = 1.41, P = 0.013) than in the control group, confirming the association of CD14 polymorphism with MI in Japanese. Stratification analyses further demonstrated that the association was more prominent in females and in patients with a relatively low body mass index, suggesting that the contribution of the CD14-linked genetic risk to MI differs with respect to gender and habitual background.
The objective of the present study was to investigate the prognostic value of plasma interleukin-8 (IL-8) for adverse cardiac events and restenosis in patients with percutaneous coronary intervention (PCI). The pre- and post-procedural peak plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, while adverse cardiac events and restenosis within one year follow-up were observed in 134 consecutive patients who underwent PCI. Angiography revealed that 23.88% (32/134) of the patients had adverse cardiac events and 29.41% (35/119) of the patients had restenosis. Preprocedural levels of IL-8 and CRP and post-procedural peak levels of IL-8 in patients with adverse cardiac events were higher than those without adverse cardiac events (all P < 0.05). The incidence of adverse cardiac events increased from 6.67% in the bottom tertile to 31.82% in the top tertile of IL-8 levels (P = 0.001); a similar trend was observed for restenosis from 10% in low tertile to 51.28% in high tertile of IL-8 levels to 51.8% (P = 0.012). The preprocedural levels of IL-8 (RR = 5.539, CI = 1.720-17.887, P = 0.001) and CRP (RR= 2.031, CI = 1.132-2.049, P = 0.003) were the only independent predictors of adverse cardiac events. The post-procedure peak level of IL-8 (RR = 3.766, CI = 2.990-5.904, P = 0.002) and stent length (RR = 1.468, CI = 1.161-2.022, P = 0.021) were the independent predictors of restenosis. The results demonstrate that the release of IL-8 after PCI is a powerful prognostic factor for cardiac events and restenosis. The higher the peak level of post-procedure IL-8, the lower the event-free survival observed.
There is epidemiologic evidence that the prognosis of patients with nonischemic heart failure is better than that for patients with ischemic heart failure. In addition, studies have revealed that patients with ischemic heart failure show a poorer response to medical therapy. However, the pathophysiologic difference between ischemic and nonischemic heart disease is unclear. To clarify this point, we measured atrial natriuretic peptide, brain natriuretic peptide, angiotensin II, endothelin (ET)-1, interleukin-1β, interleukin-6, tumor necrosis factor (TNF)-α, soluble TNF receptor I, and soluble TNF receptor II concentrations in plasma and pericardial fluid in patients with ischemic or nonischemic heart disease undergoing cardiac surgery. The pericardial ET-1 concentration in patients with ischemic heart disease was statistically greater than that in patients with nonischemic heart disease (about 1.5-fold), although no difference was found in the plasma ET-1 concentration. These findings suggest that the production and secretion of ET-1 from the myocardium in patients with ischemic heart disease are augmented to a greater extent than in patients with nonischemic heart disease. This result may lead to a greater understanding of the pathophysiology of ischemic heart disease.
Impaired heart rate variability (HRV) has been described postoperatively. Diminished HRV may be related to myocardial ischemia and potentially causes circulatory instability Cardiac ischemic events and a compromised cardiovascular function are not uncommon after aortic surgery. Circadian variation of HRV seems to be a prognostically more important parameter than HRV itself with respect to the development of cardiac dysfunction. We therefore investigated whether the diurnal rhythm of HRV is simultaneously altered postoperatively and the potential contribution of myocardial ischemia. After approval by the hospital ethics committee and having obtained informed consent, we studied 11 consecutive male patients undergoing elective aortic surgery. Patients were monitored with a Holter-ECG perioperatively. Spectral HRV measures (total, low, and high frequency power) were determined and night/day ratios calculated. Ischemic ECG changes were recorded and serum was sampled for troponin T analysis. A remarkable decline in circadian variation accompanied the decrease in all HRV parameters postoperatively. Five patients showed ECG changes suggestive of myocardial ischemia and two had increased levels of troponin T. These two patients showed greatly diminished HRV postoperatively with a similarly reduced circadian rhythm. We have demonstrated that the circadian rhythm of HRV is not preserved after aortic surgery. Diminished diurnal variability seems to be a general manifestation and myocardial ischemia may just be one contributing factor. An altered biorhythm in combination with stress related changes in the neuroendocrine system after surgery most likely have a more significant influence on the circadian rhythm of HRV.
Atrioventricular nodal reentrant tachycardia (AVNRT) is a relatively common paroxysmal supraventricular tachycardia. This study investigated whether adenosine-5'-triphosphate (ATP) injection during sinus rhythm might be useful in the noninvasive diagnosis of dual AV nodal pathways. The study group consisted of 9 patients with slow/fast AVNRT and 11 control patients without antegrade dual AV nodal physiology (DAVNP). ATP (2.5 to 30 mg, in 2.5-mg increments) was injected during sinus rhythm until signs of DAVNP (≥ 50 msec increase or decrease in AH or PR interval in two consecutive beats) or ≥ second-degree AV block was observed. DAVNP was diagnosed by ATP test in all 9 patients with slow/fast AVNRT. DAVNP was observed by ATP test in 3 of the 11 control patients. Thus, the test had a sensitivity of 100% and specificity of 73%. ATP test given during sinus rhythm is useful for identifying patients with dual AV nodal pathways who are prone to AVNRT.
Idiopathic ventricular tachycardia is rare, especially in infants. We report here on an 8month-old female infant who presented with tachycardia with a heart rate of 186 beats/min. An electrocardiogram showed a right bundle branch block pattern, a QRS duration of 80 msec, a superior QRS axis, atrioventricular dissociation, and occasional fusion and capture beats. Suspected ventricular tachycardia was treated with lidocaine, propranolol and amiodarone, but in vain. The tachycardia was terminated and well controlled with the use of verapamil. According to an electrocardiogram and her clinical response, verapamil-sensitive idiopathic ventricular tachycardia was diagnosed with the arrhythmic origin in the left posterior fascicle.
Intracardiac echocardiography (ICE) serves as an adjunct to fluoroscopy for electrophysiological procedures by identifying critical anatomic landmarks and confirming catheter-endocardial contact. In the present study, we investigated the usefulness of ICE for radiofrequency catheter ablation. ICE was utilized to guide transseptal puncture in 19 patients undergoing radiofrequency catheter ablation. The fossa ovalis, which was one critical anatomic landmark, had an average vertical diameter of 18.5 ± 6.9 mm and an average horizontal diameter of 10.0 ± 2.4 mm, as measured by ICE and fluoroscopy. Although there was only a small shift of the puncture site in the horizontal direction, the puncture site shifted towards the upper edge of the fossa ovalis for 17 patients (89%). Furthermore, we could verify that the distance between the apex of the tent-shape formed by the pressure of the puncture needle in the fossa ovalis and the left atrial wall opposing it was sufficient to carry out the procedure safely. Confirming the puncture site using ICE is useful in carrying out transseptal left heart catheterization safely.
The effects of spironolactone or metoprolol added to a conventional treatment protocol on QT dispersion, which is accepted as a sudden cardiac death predictor, were evaluated in heart failure patients.? A total of 105 New York Heart Association class III patients were included in this study. The conventional treatment protocol was standardized by giving ramipril, furosemide, and digoxin to all patients for 3 weeks at the same doses. At the end of this period, the patients were divided into three groups. Conventional treatment was continued in group 1, 25 mg spironolactone was added in group 2, and 12.5 mg metoprolol was added in group 3. Patients were followed for 12 weeks and clinical and laboratory tests were conducted at 3 week intervals. No significant change in corrected QT dispersion was observed in group1 at the end of 12 weeks (corrected QT dispersion: 80 ± 2 msc to 79 ± 2 msc, P: 0.22). However, corrected QT dispersion in group 2 was reduced by 32.5% (83 ± 2 msc to 56 ± 1 msc; P: 0.01). A 32.9% reduction in corrected QT dispersion (79 ± 2 msc to 53 ± 2 msc; P: 0.01) was observed in group 3. In conclusion, the addition of spironolactone or metoprolol to a conventional treatment in heart failure patients resulted in improved clinical conditions and the significant decrease in sudden death predictors corrected QT dispersion. The effects of spironolactone and metoprolol on corrected QT dispersion were similar.
The short term (three months) effects of rilmenidine on systemic hypertension induced left ventricular hypertrophy (LVH) and left ventricular systolic and diastolic functions in comparison with those of perindopril and nifedipine-slow release (SR) formulation were studied. The short term effects of rilmenidine on biochemical parameters and lipid profiles were evaluated. Sixty patients (39 men, 21 women) with a mean age of 59 ± 14 years and with mild to moderate systemic arterial hypertension were enrolled in three groups. The first group received 1 mg/day of rilmenidine, the second group 4 mg/day of perindopril, and the third group 20 mg/day of nifedipine SR. All drugs induced a similar decrease in systolic and diastolic blood pressure (BP) values. Left ventricular mass (LVM) and LVM index decreased equally in all groups associated with a significant increase in the E/A ratio. The ratio between the reduction in LVM and decrease in mean arterial pressure (LVM/mmHg) was higher in groups 1 and 2. Negative correlations between LVM and LVMI, E/A, and the dv/dt ratio were obtained. Rilmenidine did not change the blood chemistry and lipid profile values. Despite its neutral effect on lipid profile and biochemical parameters, rilmenidine is as effective as perindopril and nifedipine in controlling hypertension and decreasing left ventricular hypertrophy.
Mitral stenotic patients with left atrial spontaneous echo contrast (LA SEC) are associated with high risk of thromboembolism. The aim of this study was to predict thromboembolic risk in mitral stenotic patients. Femoral artery signal intensity alteration (%) was compared among the groups. Group 1 had severe mitral stenosis with LA SEC and group 2 slight mitral stenosis without LA SEC. Group 3 patients had normal transthoracic echocardiography. Femoral artery longitudinal view was studied with a linear USG probe (7.5 MHz, HP 2500). The femoral cuff was inflated to 300 mmHg, 7-12 cm below the inguinal ligament. Cuff inflation resulted in femoral arterial blood stasis. Intraluminal signal intensity increased in seconds. The femoral signal intensity alteration (%) at 180 seconds was compared to baseline. After femoral cuff inflation, femoral signal intensity alteration (%) was significantly higher in group 1 than groups 2 and 3 (P < 0.001). Group 1 patients had higher thromboembolic risk on the basis of their echocardiographic, clinical, and laboratory parameters. Increased signal intensity alteration (%) can be detected in the femoral artery in mitral stenotic patients with LA SEC.
Cyclic GMP (cGMP) serves as an intracellular second messenger of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and nitric oxide (NO) and its peripheral blood concentration is an index of its biological activity. It has been reported that the plasma concentration of cGMP is correlated with the concentrations of ANP and BNP and is related to the prognosis of chronic heart failure patients, but the relation with NO has not been studied. Therefore, we investigated the roles of ANP, BNP, and NO in relation to cGMP in the blood during worsening and improvement of chronic heart failure. The subjects were 25 patients who were hospitalized in our hospital for acute worsening of chronic heart failure. Plasma concentrations of NO, norepinephrine (NE), ANP, BNP, and cGMP were measured on acute worsening (admission) and improvement (discharge) of heart failure. The cGMP concentration on worsening showed a positive correlation with the NO concentration (r = 0.57, P < 0.01), but no correlations with ANP or BNP were observed. The cGMP concentration on improvement showed no correlation with the NO concentration, but a positive correlation with ANP (r = 0.69, P < 0.001) and BNP (r = 0.67, P < 0.001). No correlation was observed between the NO and NE concentrations. We also studied serious cases of NYHA IV and mild cases of NYHA II to III. The cGMP concentration in the serious group showed a positive correlation with the NO concentration but no correlations with ANP or BNP concentrations on worsening. However, in the mild group, the cGMP concentration during worsening showed positive correlations with both the NO and BNP concentrations. On improvement, the cGMP concentration showed no correlation with the NO concentration but positive correlations with both the ANP and BNP concentrations in both the severe and mild groups. The results suggest the possibility that cGMP is produced mainly by NO during worsening, and by ANP and BNP rather than NO during improvement of chronic heart failure.
Chronic heart failure (CHF) is characterized by the activation of neurohormones and cytokines. This study determined whether peak oxygen uptake (VO2) can be predicted by the degree of neurohormonal and cytokine activations in CHF. Plasma norepinephrine, epinephrine, renin-angiotensin system activity, ANP, BNP, and serum interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α were measured in 84 CHF patients (age, 59 ± 1 years, LVEF, 36 ± 1%) and 34 controls. Maximal cardiopulmonary exercise testing was performed. Peak VO2 (Controls vs CHF: 27.8 ± 1.3 vs 18.2 ± 0.5 mL/min/kg, P < 0.0001) was lower in CHF. Patients with CHF had increased plasma norepinephrine (211 ± 11 vs 315 ± 24 pg/mL), renin activity (1.2 ± 0.2 vs 6.2 ± 1.1 ng/mL/hr), ANP (22 ± 3 vs 72 ± 7 pg/mL), and BNP levels (18 ± 3 vs 200 ± 25 pg/mL) (all P < 0.01). Serum IL-6 (1.1 ± 0.1 vs 2.4 ± 0.3 pg/mL) and TNF-α (2.7 ± 0.2 vs 4.0 ± 0.3 pg/mL) levels were higher in CHF (both P < 0.001). Univariate analysis revealed that age (P < 0.001), cardiothoracic ratio (P < 0.001), norepinephrine (P < 0.0001), ANP (P < 0.001), BNP (P < 0.01), and log IL-6 (P < 0.05) were significantly related with peak VO2. Stepwise regression analysis indicated that plasma norepinephrine and ANP emerged as significant determinants of peak VO2, independent of patient age (overall R = 0.61, P < 0.0001). In summary, patients with CHF exhibited activation of neurohormones and proinflammatory cytokines. Among the elevated hormonal and cytokine markers, plasma norepinephrine and ANP levels were independent predictors of exercise capacity.
For the management of chronic heart failure, both angiotensin converting enzyme inhibitors (ACEI) and angiotensin II type1 receptor blockers (ARB) are useful, however, the differences between the two groups of agents are unclear. We compared the effects of long-term treatment with an ACEI (imidapril) and an ARB (TA-606) in rats that had recovered from experimental autoimmune myocarditis (EAM). Forty-two Lewis rats were immunized with porcine cardiac myosin on day 0 and divided into 6 groups, group C (distilled water), group IL (imidapril 0.5 mg/kg/day), group IH (imidapril 2 mg/kg/day), group TL (TA-606 2 mg/kg/day), group TH (TA-606 6 mg/kg/day), and group IT (imidapril 0.5 mg/kg/day + TA-606 2 mg/kg/day). Drugs were administered from day 28. Hemodynamic parameters, heart weight/body weight ratio (HW/BW), and area of fibrosis were measured on days 70-74. Only the high dose of imidapril significantly decreased central venous pressure and significantly increased maximum dP/dt and the absolute value of minimum dP/dt. HW/BW was suppressed in groups IH, TH, and IT. Thus, in treatment of chronic heart failure in rats, a sufficient dose of ACEI was needed to improve hemodynamics and to prevent ventricular hypertrophy. The hemodynamic effects of ARB and combination therapy of both drugs at low doses were not significant.
Vanadium mimicking the metabolic effects of insulin is known to decrease serum glucose levels and to influence glucose metabolism in diabetes mellitus. However, it is unclear whether vanadium ameliorates the metabolic disorder in diabetic hearts causing myocardial dysfunction. The purpose of this study was to assess the effects of vanadium on cardiac performance and energy metabolism in diabetic rat hearts. Four groups of Wistar rats were studied: untreated control rats (group C, n = 8), vanadate-treated rats (group V, n = 10), untreated diabetic rats (group DM, n = 9) induced by streptozotocin, and vanadate-treated diabetic rats (group DMV, n = 8). Vanadate-treated rats drank a 1.5 mM sodium orthovanadate (Na3VO4) solution during a 4 week diabetic condition. Hearts were perfused with Krebs-Henseleit buffer after the diabetic duration. After the maximum left ventricular dP/dt and cardiac efficiency were calculated, the myocardial contents of ATP and creatine phosphate (P-Cr) and myocardial energy metabolism were assessed by cytosolic phosphorylation potential. Peak positive and negative dP/dt, and cardiac efficiency decreased significantly in group DM compared with group C, while there were no significant differences between groups C and DMV. The myocardial contents of ATP (μmol/g wet heart) and P-Cr (μmol/g wet heart), and cytosolic phosphorylation potential (M-1) increased from 2.72 ± 0.46, 1.45 ± 0.58, and 3,530 ± 1,220 in group DM to 3.88 ± 0.76, 3.81 ± 1.36, and 11,200 ± 2,400 in group DMV, respectively. It is concluded that vanadium restored the production of high energy phosphates in the myocardium and improved myocardial dysfunction by regulating metabolic processes in diabetic rat hearts.
We report 2 cases with an isolated single coronary artery who underwent successful primary coronary intervention for acute coronary syndrome. Although coronary angioplasty with stenting may be a feasible therapeutic option for atherosclerotic stenosis in a single coronary artery, the operator should be aware of the potential risk of complications.
Cholesterol crystal embolization (CCE) is a complication of atherosclerosis. A 67-year-old Japanese man underwent coronary artery bypass grafting. After the surgery, he underwent coronary angiography via the right femoral artery. Twelve days later, he suddenly developed acalculous cholecystitis and was treated with antibiotics. Gradual deterioration in renal function, purplish discoloration of the distal portion of his toes, and eosinophilia were noted. We performed a skin biopsy and made a diagnosis of CCE. Cilostazol and intravenous heparin improved the symptoms and decreased the creatinine level. We retrospectively studied the clinical features of 36 cases registered with a diagnosis of CCE in the Japanese literature.
Two brothers had familial hypertrophic cardiomyopathy and vasospastic angina pectoris concurrently. Their family history showed that one of their sisters had hypertrophic cardiomyopathy and another brother died suddenly at age 52. The clinical diagnosis of hypertrophic cardiomyopathy was confirmed by an echocardiogram and left ventriculo-graphy. They had typical chest pain at rest, and a significant vasospasm of coronary arteries with chest pain and obvious ST-T changes in the elctrocardiograms was provoked by intracoronary injection of acetylcholine in both patients. The administration of a calcium antagonist and nitrate was effective for ameliorating chest pain with no cardiovascular events during the follow up period of more than 3 years. Although underlying pathophysiologic abnormalities of familial hypertrophic cardiomyopathy and vasospastic angina pectoris are considered to be transmitted genetically, the genetic backgrounds of these cases remain to be clarified.
A 65-year-old Japanese woman was admitted to hospital because of palpitations and faintness. She was diagnosed as having sick sinus syndrome and a permanent pacemaker was therefore implanted. Administration of bepridil (200 mg daily) was started for prevention of atrial flutter and fibrillation after PM implantation. On the twenty-fifth day of Bpd therapy, she developed recurrent syncope. ECG showed QT prolongation, torsades de pointes, and sensing failure. Electrical defibrillation (DF) was performed for ventricular fibrillation or ventricular tachycardia. It was presumed that Bpd had caused not only proarrhythmia but also a transient decrease in the amplitude of ventricular activation at the site of the pacing lead, as the sensing level was gradually restored after the drug was ceased and her plasma concentrations of Bpd decreased. It is also believed that DF had caused a sustained increase in pacing threshold because she developed pacing failure after DF and her pacing threshold had not returned to its prior level although the blood levels of Bpd had been below the minimum detectable level. Although it is well known that torsades de pointes occasionally develops in association with Bpd therapy, it is less evident that pacing and sensing failure may develop in association with Bpd therapy. This case report suggests that we should be aware of this possible outcome when employing Bpd and pacemaker implantation as combination therapy.
A 70-year-old Japanese woman was admitted to our hospital because of transient second degree atrioventricular (AV) block. An electrophysiologic study (EPS) was performed, and Mobitz type II infra-Hisian block during atrial pacing at a rate of 130/min was noted. An AV nodal reentrant tachycardia (AVNRT) was induced by ventricular pacing at a rate of 180/min, and 2:1-3:1 infra-Hisian block during AVNRT was observed. The AV block and AVNRT rarely occurred in the clinical setting, and the patient did not complain of any symptoms related to these arrhythmias. Therefore, the patient refused permanent pacemaker implantation, although she continued to be followed in our outpatient clinic. However, the patient was re-admitted one year later because of palpitations and dyspnea upon exertion related to the AV block. The 12-lead ECG showed high degree AV block with narrow QRS complexes. The patient underwent pacemaker implantation during the subsequent hospitalization, and her symptoms improved postoperation. AV block during AVNRT is sometimes observed, and it has been considered as a functional AV block. In the present case, a pathologic conduction disturbance in the His-Purkinje system caused the high degree AV block during AVNRT. The high degree AV block during AVNRT may indicate the existence of a conduction disturbance in the His-Purkinje system in some of these types of cases.
A 74-year-old Japanese male was admitted to hospital with episodes of chest pain. Cross-sectional echocardiography showed a mobile mass adherent to the noncoronary cusp of the aortic valve. We employed transesophageal echocardiography and magnetic resonance imaging to evaluate the mass. Based on the findings, a papillary fibroelastoma of the aortic valve was suspected. To avoid systemic embolization, urgent surgery was performed. The histopathologic diagnosis was papillary fibroelastoma. When a tumor of the aortic valve exists, these examinations are useful in detecting and characterizing the tumor for optimal treatment.
Congestive heart failure (CHF) due to hyperkinetic states can occur in systemic diseases and in arteriovenous fistulas. An 18 year old Turkish male patient complaining of dyspnea and palpitations, who had suffered a stab wound to his abdomen eight months earlier, was admitted to our clinic. Auscultation revealed a systolodiastolic murmur over the entire abdomen. Chest x-rays demonstrated significant cardiomegaly. Echocardiography revealed biatrial enlargement and significant mitral and tricuspid regurgitation accompanied by dilatation of the inferior vena cava. Right heart catheterization showed increased oxygen saturation at the inferior vena cava. A diagnosis of an aortocaval fistula was made by aortography. The symptoms subsided and valvular regurgitations ceased after surgical correction. This rare case demonstrates the significance of routine physical examination and history of the patient.