Time course of recovery of left ventricular systolic dysfunction in patients with premature ventricular contraction-induced cardiomyopathy.

BACKGROUND: Idiopathic ventricular arrhythmias in the form of frequent, monomorphic premature ventricular contractions (PVC) can cause PVC-induced cardiomyopathy (PICMP). The aim of this study was to determine the baseline echocardiographic characteristics and the time course and degree of recovery of left ventricular (LV) systolic dysfunction in patients with PICMP. METHODS: Study population consisted of 348 consecutive patients (205F/143M, 44 ± 19 y/o) with frequent PVCs and/or ventricular tachycardia. PICMP was defined as LV ejection fraction (LVEF) of <55% in the absence of any detectable underlying heart disease and improvement of LVEF ≥ 15% following treatment of ventricular arrhythmia. Patients with PCIMP underwent transthoracic echocardiography for LV size and function at 1 week and at 1-3 to 6-12 months of follow-up. RESULTS: Twenty-four patients (8F/16M, 47 ± 18 y/o) with PICMP with complete echocardiographic data were included in the study. Average baseline LV end-diastolic diameter, LV end-systolic volume, LV mass index, and LVEF were 55.4 ± 6.8 mm, 69.6 ± 23.3 mL, 110.2 ± 28.3 g/m2, and 41 ± 8.4%, respectively. Mild-to-moderate mitral regurgitation (MR) was present in 13 (54%) patients. Early improvement (≥25% increase in LVEF at 1-week follow-up compared to baseline) was observed in 13 (54%) patients. Patients with early improvement had higher LVEF at 12 months of follow-up compared to patients without early improvement (58.8 ± 5.0% vs 52.5 ± 6.7%, P = 0.019). CONCLUSIONS: PCIMP is characterized by mild-to-moderate global LV systolic dysfunction with slightly increased LV mass and mild-to-moderate MR. Greatest improvement in LV systolic dysfunction was observed at 1-week follow-up in our study population. Early improvement in LVEF may potentially predict the complete reversibility of LV systolic dysfunction.

Chronic cough and tachycardia-induced cardiomyopathy in a patient with idiopathic frequent, monomorphic premature ventricular contractions.

A 70-year-old woman presented with a 1-year history of dry cough. Extensive work-up ruled out common causes of chronic cough. She was found to have very frequent, monomorphic premature ventricular contractions (PVCs) and mild-to-moderate left ventricular systolic dysfunction. Propafenone 450 mg/day resulted in complete resolution of her cough and disappearance of PVCs within 24 hours of initiation. One month after the initiation of propafenone therapy, left ventricular ejection fraction normalized and her chronic cough resolved completely.

Cardiac resynchronization therapy with or without anatomical reverse remodeling does not affect defibrillation threshold.

BACKGROUND: Recent clinical trials have documented beneficial reverse-remodeling effects with cardiac resynchronization therapy (CRT). The aim of this study was to investigate the effect of CRT with or without reverse anatomical remodeling of the left ventricle on defibrillation threshold (DFT) levels in a prospective and consecutive group of patients with class II-IV systolic heart failure. METHODS: Study population consisted of 29 patients (14 women and 15 men; mean age 61±11 years old). All patients underwent baseline (within 24-hours of cardiac resynchronization therapy-defibrillator [CRT-D] implantation) and 6-month follow-up DFT testing. Reverse anatomical remodeling of the left ventricle was defined as ≥15% reduction in left ventricular end-systolic volume at the end of 6 months of follow-up compared to baseline. RESULTS: Baseline, average DFT was 8.8±5.9 J. Left ventricular end-diastolic volume was the only predictor of baseline DFT level (P=0.02) among the baseline demographics. Safety margin of at least 10 J was achieved in all patients. Average DFT at the end of 6 months of biventricular pacing was 9.2±6.9 J. One patient (3.4%) failed to have a safety margin of 10 J. Reverse anatomical remodeling was observed in 14 (48%) patients and did not have any effect on DFT level. There were no complications related to DFT testings. CONCLUSIONS: Baseline average DFT in patients undergoing CRT-D was ≤10 J in our study. CRT-D with or without anatomical reverse remodeling does not affect DFT at the end of 6 months of follow-up. High DFT level at the end of 6 months of follow-up is rare (3.4%) among patients with current CRT-D devices.

Late gadolinium enhancement CMR in patients with tachycardia-induced cardiomyopathy caused by idiopathic ventricular arrhythmias.

BACKGROUND: Idiopathic ventricular arrhythmias in the form of monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) can cause tachycardia-induced cardiomyopathy (TICMP). The aim of this study was to determine the prevalence of late gadolinium enhancement (LGE) in patients with TICMP caused by idiopathic ventricular arrhythmias. METHODS: The study population consisted of 298 consecutive patients (174 F/124 M; mean age 45±17 years) with frequent PVCs and/or VT. TICMP was defined as left ventricular ejection fraction (LVEF) of ≤50% in the absence of any detectable underlying heart disease and improvement of LVEF≥15% after effective treatment of index ventricular arrhythmia. RESULTS: Twenty-seven (9.1%) patients found to have LVEF≤50% and diagnosed as presumptive TICMP. Improvement in LVEF after effective treatment of index ventricular arrhythmia was observed in 22 of 27 patients (TICMP group; mean PVC burden of 30.8±9.9%). LVEF did not improve in five of 27 patients (primary cardiomyopathy group; mean PVC burden of 28.8±10.1%). LGE-cardiac magnetic resonance (CMR) imaging was performed in 19 of 22 patients with TICMP and one patient (5%) had LGE. All five patients with primary cardiomyopathy underwent LGE-CMR imaging and four patients (80%) had LGE. CONCLUSIONS: LGE is a rare finding in patients with TICMP caused by idiopathic ventricular arrhythmias. LGE-CMR can be used in the diagnostic work-up of patients with TICMP. Further prospective studies are required to determine the role of LGE-CMR in predicting the recovery of left ventricular systolic dysfunction in patients with presumptive TICMP.

Tachycardia-induced cardiomyopathy in patients with idiopathic ventricular arrhythmias: the incidence, clinical and electrophysiologic characteristics, and the predictors.

INTRODUCTION: Idiopathic ventricular arrhythmias in the form of monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) can cause tachycardia-induced cardiomyopathy (TICMP). The aim of this study was to determine the incidence, clinical and electrophysiologic characteristics, and the predictors of TICMP in patients with idiopathic ventricular arrhythmias. METHODS: Study population consisted of 249 consecutive patients (148 F/101 M, 45 ± 20 y/o) with frequent PVCs and/or VT. All patients underwent transthoracic echocardiography and 24-hour Holter monitoring. TICMP was defined as left ventricular ejection fraction (LVEF) of ≤50% in the absence of any detectable underlying heart disease and improvement of LVEF ≥15% following effective treatment of index ventricular arrhythmia. RESULTS: Seventeen (6.8%) patients had TICMP. Patients with TICMP compared to patients with preserved LVEF were more likely to be male (65% vs 39%, P = 0.043) and asymptomatic (29% vs 9%, P = 0.018), and were more likely to have higher PVC burden (29.4 ± 9.2 vs 8.1 ± 7.4, P < 0.001), persistence of PVCs throughout the day (65% vs 22%, P = 0.001), and repetitive monomorphic VT (24% vs 0.9%, P < 0.001). PVC burden of 16% by ROC curve analysis best separated the patients with TICMP compared to patients with preserved LVEF (sensitivity 100%, specificity 87%, area under curve 0.96). CONCLUSIONS: TICMP was relatively common (∼1 in every 15 patients) in our study population. The predictors of TICMP were male gender, absence of symptoms, PVC burden of ≥16%, persistence of PVCs throughout the day, and the presence of repetitive monomorphic VT.

Left atrial volume predicts mortality in low-risk dialysis population on long-term low-salt diet.

BACKGROUND: Echocardiography provides insight to the management of end-stage renal disease (ESRD) and might be valuable in assessing the prognosis. We evaluated the predictive value of echocardiography along with clinical findings in a low-risk hemodialysis (HD) population who had been treated with strict salt restriction strategy for blood pressure control. METHODS: Study population consisted of a cohort of 555 ESRD patients from 8 HD centers where the same strict volume control strategy applied for blood pressure control. Clinical findings and echocardiography were examined as predictors of mortality for a mean follow-up period of 3 years (29.6 +/- 11.6 months). RESULTS: During the follow-up, 89 patients (16%) died. Left atrium (LA) volume index was the only independent echocardiographic predictor of mortality (hazard ratio 1.025, 95% CI 1.001-1.050, P = .042). The other predictors of mortality were age, pulse pressure, diabetes mellitus, and high-sensitivity C-reactive protein. However, when we added interdialytic weight gain (IDWG) ratio to the Cox model, it also appeared as an independent predictor of mortality, whereas LA volume index no longer was. CONCLUSIONS: Increased LA volume index emerged as the only independent echocardiographic determinant of mortality in low-risk dialysis patients treated by strict volume control. Close relationship with IDWG ratio indicates the intermittent stretching of atrium between dialysis sessions leading to atrial remodeling. This index is not the result of a single factor such as age, hypervolemia, or left ventricular hypertrophy but reflects the combination of these contributing causes. Therefore, it might be considered as an overall echocardiographic sign of mortality in ESRD.

Transcriptional profiling of septal wall of the right ventricular outflow tract in patients with idiopathic ventricular arrhythmias.

BACKGROUND: Frequent, monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) in patients with structurally normal heart usually arise from the right ventricular outflow tract (RVOT). The underlying arrhythmogenic substrate for the genesis of RVOT tachycardias is largely unknown. The aim of this study was to investigate the genome-wide transcriptional profiling of the septal wall of the RVOT in patients with RVOT tachycardia and control subjects. METHODS: Transcriptional profiling with Affymetrix 3' IVT microarray analysis (Affymetrix, Santa Clara, CA, USA) was performed on the endomyocardial biopsy samples obtained from the septal wall of the RVOT from three unrelated patients with RVOT tachycardia and three control subjects. All study subjects had normal right and left ventricular size and function. Microarray results were validated by real time polymerase chain reaction (PCR). RESULTS: There were 32 statistically significant up-regulated and 60 down-regulated genes in five biological networks in patient population compared with control subjects. Among those genes, there were eight down-regulated [ATP1A2, CACNA1C, Protein Phosphatase 2, Regulatory Subunit B, Gamma Isoform[PPP2R2C], PLCD3, GNAO1, Solute Carrier Family 6 (Transporter, Norepinephrine), Member 2(SLC6A2), CAMK2B, PIK3R2] and two up-regulated (CAMKK2 and ITPR3) genes related to myocardial intracellular calcium regulation. In addition, there were five down-regulated [T-box 3(TBX3), Bone Morphogenetic Protein 2(BMP2), Bone Morphogenetic Protein Receptor, Type IB(BMPR1B), MYH6, Ankyrin Repeat Domain 23 and 39(ANKRD23-39)] and one up-regulated gene (RGS1) related to cardiovascular functions. CONCLUSION: The expression of genes responsible for the regulation of myocardial intracellular calcium and the development of RVOT are significantly down-regulated in the septal wall of the RVOT in patients with RVOT tachycardia compared with control subjects.

Termination of idiopathic sustained monomorphic ventricular tachycardia by intravenous adenosine in a pregnant woman.

A 34-year-old pregnant woman presented to the emergency department with the complaints of palpitations at 32 weeks gestation. The diagnosis of right ventricular outflow tract ventricular tachycardia (VT) was made. Intravenous 5 mg of metoprolol and 25 mg of diltiazem did not terminate the VT. Ten milligrams of adenosine were administered. Within 10 s of adenosine administration, sustained VT converted to repetitive monomorphic VT and within 30 s to normal sinus rhythm. The mother and the foetus tolerated the medications well. Non-stress test for the assessment of the foetal well-being was normal.

Successful balloon dilatation of the valve of Vieussens for left ventricular lead placement.

Successful balloon dilatation of an obstructive valve of Vieussens for left ventricular lead placement is described in a case with severe left ventricular systolic dysfunction.

Human model simulating right ventricular outflow tract tachycardia by high-frequency stimulation in the left pulmonary artery: autonomics and idiopathic ventricular arrhythmias.

INTRODUCTION: Frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) in patients with structurally normal heart usually arise from the right ventricular outflow tract (RVOT). An animal model simulating RVOT tachycardia by high-frequency stimulation (HFS) of the sympathetic input to the proximal pulmonary artery (PA) has been previously described. The aim of this study was to similarly induce RVOT tachycardia in humans. METHODS: In 9 patients with no history of ventricular arrhythmias, a circumferential catheter was placed in the left, main, and proximal PA to contact the endovascular circumference of the PA. A 50-ms train of HFS (200 Hz/0.3 ms pulse duration), coupled to atrial pacing, was applied at each bipolar pair of the circumferential catheter. The coupling interval was adjusted so that the 50-ms train occurred during the ventricular refractory period. RESULTS: In 6 out of 9 patients, HFS in the left PA during dobutamine infusion induced monomorphic PVCs and/or VT with left bundle branch block (LBBB) morphology and inferior axis at an average stimulation level of 12.5 +/- 2.7 V. HFS in the main PA and in the proximal PA did not induce any ventricular arrhythmias with the highest energy of 15 V in baseline state and during dobutamine infusion. HFS in the left PA was associated with hiccough in all patients. CONCLUSION: Stimulation of the sympathetic input to the left PA during dobutamine infusion induces PVCs and/or VT exhibiting LBBB-morphology and inferior axis, closely simulating clinical RVOT tachycardia in humans.

The benefit of salt restriction in the treatment of end-stage renal disease by haemodialysis.

BACKGROUND: Most haemodialysis (HD) centres use anti-hypertensive drugs for the management of hypertension, whereas some centres apply dietary salt restriction strategy. In this retrospective cross-sectional study, we assessed the effectiveness and cardiac consequences of these two strategies. METHODS: We enrolled all patients from two dialysis centres, who had been on a standard HD programme at the same centre for at least 1 year. All patients underwent echocardiographic evaluation. Clinical data were obtained from patients' charts. Centre A (n = 190) practiced 'salt restriction' strategy and Centre B (n = 204) practiced anti-hypertensive-based strategy. Salt restriction was defined as managing high blood pressure (BP) via lowering dry weight by strict salt restriction and insistent ultrafiltration without using anti-hypertensive drugs. RESULTS: There was no difference regarding age, gender, diabetes, history of cardiovascular disease and efficiency of dialysis between centres. Antihypertensive drugs were used in 7% of the patients in Centre A and 42% in Centre B (P < 0.01); interdialytic weight gain was significantly lower in Centre A (2.29 +/- 0.83 kgversus 3.31 +/- 1.12 kg, P < 0.001). Mean systolic and diastolic blood pressures were similar in the two centres. However, Centre A had lower left ventricular (LV) mass (indexed for height(2.7): 59 +/- 16 versus 74 +/- 27 g/m(2.7), P < 0.0001). The frequency of LV hypertrophy was lower in Centre A (74% versus 88%, P < 0.001). Diastolic and systolic functions were better preserved in Centre A. Intradialytic hypotension (hypotensive episodes/100 patient sessions) was more frequent in Centre B (11 versus 27, P <0.01). CONCLUSIONS: This cross-sectional study suggests that salt restriction and reduced prescription of antihypertensive drugs may limit LV hypertrophy, better preserve LV functions and reduce intradialytic hypotension in HD patients.

Increased myocardial collagen turnover in patients with progressive cardiac conduction disease.

BACKGROUND: Histopathologically, progressive cardiac conduction disease (PCCD) is characterized by progressive fibrosis and sclerodegenerative changes in the proximal and distal conduction system of the heart. Therefore, we sought to determine the serum levels of myocardial collagen turnover markers, extracellular matrix components, transforming growth factor beta(1) (TGFbeta(1)), and bone morphogenic protein-7 (BMP-7) in this population. METHODS: Study population included 20 patients (6 M/14 F, mean age 76 +/- 8 years) with acquired, permanent 2:1, or complete atrioventricular block and compared with age- and sex-matched, asymptomatic, healthy control subjects (n = 18, 6 M/12 F, mean age 75 +/- 7 years). Serum myocardial collagen turnover markers:matrix metalloproteinases (MMP-1, 2, 9), tissue inhibitor of matrix metalloproteinase (TIMP-1), amino-terminal propeptide of procollagen type I (PINP) and type III (PIIINP), carboxy-terminal telopeptide of collagen type I (CITP), and carboxy-terminal propeptide of procollagen type I (PICP), serum extracellular matrix components (laminin and fibronectin), TGFbeta(1), and BMP-7 levels were measured in both groups. RESULTS: Serum PICP (849 +/- 396 vs 631 +/- 294 ng/mL, P = 0.04), PIIINP (3.7 +/- 1.3 vs 3 +/- 1 mug/L, P = 0.03), CITP (0.68 +/- 0.35 vs 0.48 +/- 0.25 ng/mL, P = 0.037), and plasma MMP-9 (58.8 +/- 56 vs 25.9 +/- 17.3 ng/mL, P = 0.006) levels were higher in patient population compared to control subjects. Serum MMP-1 (24.1 +/- 20.5 vs 13.6 +/- 7.5 ng/mL, P = 0.045) and MMP-2 (1310 +/- 139 vs 1186 +/- 163 ng/mL, P = 0.01) levels were higher in control subjects compared to patient population. There was no difference in serum TIMP-1, PINP, laminin, fibronectin, TGFbeta(1), and BMP-7 levels between two groups. CONCLUSION: Our findings demonstrate the presence of increased myocardial collagen turnover and active fibrotic process in patients with PCCD compared to control subjects.

Beta1 and beta2-adrenergic receptor polymorphisms and idiopathic ventricular arrhythmias.

INTRODUCTION: Idiopathic ventricular arrhythmias commonly refer to ventricular tachycardia (VT) and/or frequent/monomorphic premature ventricular contractions (PVC) in patients with structurally normal heart. Activation of sympathetic tone has been shown to play an important role in the provocation and maintenance of these arrhythmias. We investigated whether common single nucleotide polymorphisms in the beta(1) and beta(2)-adrenergic receptors are associated with idiopathic ventricular arrhythmias. METHODS: A total of 143 unrelated patients presenting with idiopathic ventricular arrhythmias were prospectively included in a case-control association study. Patient population was matched by age and gender to the unrelated, healthy control subjects (N = 307). All study subjects were of Turkish (Anatolian Caucasian) descent. Allele and genotype frequencies of the Gly389Arg and Ser49Gly polymorphisms of the beta(1)-adrenergic receptor and Arg16Gly, Gln27Glu, and Thr164Ile polymorphisms of the beta(2)-adrenergic receptor were compared between patient population and control subjects. The genotype frequencies were in Hardy-Weinberg equilibrium. RESULTS: Patients with idiopathic ventricular arrhythmias had higher frequency of Arg389Arg genotype (22.4% vs 1.6%, P < 0.001), Arg389Gly49 (5.24% vs 0.73%, P = 0.005), and Arg389Ser49 (36.7% vs 13.6%, P < 0.001) haplotypes of the beta(1)-adrenergic receptor, and higher frequency of Gly16Gly (31.5% vs 13.4%, P < 0.001), Glu27Glu genotypes (18.2% vs 10.1%, P = 0.006) and Gly16Gln27Thr164 (15.3% vs 7.4%, P = 0.002), Gly16Glu27Thr164 (13.1% vs 7%, P = 0.004), and Gly16Glu27Ile164 (13.2% vs 6%, P = 0.002) haplotypes of the beta(2)-adrenergic receptor compared to control subjects. CONCLUSION: Our data suggest that common single nucleotide polymorphisms in the beta(1) and beta(2)-adrenergic receptors are significantly associated with idiopathic ventricular arrhythmias in Turkish population.

Repolarization characteristics and incidence of Torsades de Pointes in patients with acquired complete atrioventricular block.

OBJECTIVE: Torsades de pointes (TdP) during bradyarrhythmias have been reported to be associated with gender, degree of QT prolongation and duration of bradyarrhythmia. We sought to investigate the repolarization characteristics on 12-lead electrocardiogram (ECG) and the incidence of TdP in patients with acquired complete atrioventricular block (CAVB). METHODS: Fifty consecutive patients with acquired CAVB were included in the study. Patients with coronary artery disease, systolic dysfunction and previous cardiac surgery were excluded. Patients were monitored during hospitalization for ventricular arrhythmias (VA). Serum potassium, magnesium, calcium levels and thyroid-stimulating hormone were measured. Heart rate, QRS duration, QT/QTc, JT/JTc and Tpeak-Tend intervals were measured. Pathologic U waves, T-U complex, and QT morphologies were remarked. RESULTS: Patients presented with presyncope (n=39, 78%), syncope (n=12, 24%), and palpitations (n=8, 16%). All patients were in sinus rhythm. Duration of CAVB was 8.5 days (median). Patients were divided into two groups based on JT interval. Group 1 (JT=or>500 ms, n=13) tended to have more female patients and more VAs in comparison to Group 2 (JT<500 ms, n=37). Group 1 patients had more pathologic U waves and T-U complexes, longer Tpeak-Tend intervals, and more long QT2 syndrome (LQT2)-like QT morphology in comparison to Group 2 patients. Group 2 patients had more often syncope. One patient in Group 2 developed ventricular fibrillation in the presence of hypokalemia and hypomagnesemia. CONCLUSION: Torsades de Pointes during CAVB was rare among our patient population. The predictors of VA during CAVB were presence of prolonged QTc/JTc intervals, pathologic U wave and T-U complex, prolonged Tpeak-Tend interval, and LQT2-like QT morphology.

Angiographic analysis of the anatomic relation of coronary arteries to mitral and tricuspid annulus and implications for radiofrequency ablation.

Coronary artery (CA) narrowings and/or occlusions after radiofrequency ablation (RFA) have been reported. The aim of this study was to describe the in vivo topographic anatomy of CAs and their anatomic relation to the mitral and tricuspid annulus using selective coronary angiography. Fifty consecutive patients undergoing RFA for narrow QRS complex tachycardia were included in the study. Multipolar electrode catheters were inserted into the right atrial appendage, His bundle region, distal coronary sinus (CS), and right ventricle. A mapping catheter was placed across the subeustachian isthmus (SEI). Selective coronary angiography was performed. The maximum and minimum distances between the distal CAs and the mapping catheter located along the mitral and tricuspid annulus were measured during systole and diastole and in right and left anterior oblique projections. The large (> or =1.5 mm) distal right CA was < or =5 mm from the mapping catheter in the SEI in 4 patients (8%). The large posterolateral branch of the right CA was < or =2 mm from the CS Os-middle cardiac vein in 10 patients (20%). The large left circumflex CA was < or =2 mm from the floor or ceiling of the CS in 7 patients (14%) and < or =2 mm from the CS catheter at the lateral and anterolateral mitral annulus in 12 patients (24%). RFA was canceled in 2 patients because of the close proximity (< or =2 mm) of the distal CA to the ablation site. In conclusion, large CAs are frequently located in close proximity to the common ablation sites. Coronary angiography should be considered in children and adults who may develop any signs or symptoms suggestive of acute CA occlusion until larger controlled series are available.

Serum paraoxonase 1 activity and oxidative markers of LDL in patients with cardiac syndrome X.

OBJECTIVE: Myocardial ischaemia in cardiac syndrome X (CSX) is believed to be due to microvascular dysfunction. Increased oxidative stress is one of the suspected mechanisms of microvascular dysfunction. The aim of this study was to evaluate the oxidative status in patients with CSX, by determining serum paraoxonase-1 (PON 1) activity in addition to LDL-oxidation markers. METHODS AND RESULTS: This cross-sectional study consisted of patients with CSX (group I, n = 30), patients with coronary artery disease (group II, n = 31), and healthy controls (group III, n = 32). Lipid parameters, PON-1 activity, and LDL oxidation markers (conjugated-diene and thiobarbituric acid-reactive substance-TBARS) were measured. Endothelium-dependent vasodilatation was determined by brachial artery ultrasonography. There were no significant differences in serum LDL, apolipoprotein-B, baseline LDL-diene, and LDL-TBARS levels between groups. There were no differences in both apolipoprotein-A1 and HDL levels between group I and group III. Apolipoprotein-A1 and HDL levels were significantly lower in group II than group I patients (P < 0.001). PON-1 activity was lowest in group II patients. Average PON-1 activity in group I was in between of group II and group Ill. The percent change of LDL-diene levels after stimulation was significantly higher in group II than in groups I and III (P = 0.005 and P = 0.02, respectively). The percent change of LDL-TBARS levels was lowest in group I (P = 0.03). There was a moderate correlation between endothelium-dependent vasodilatation and PON-1 activity in group I (r = 0.43, P = 0.04). CONCLUSIONS: Enhanced oxidative stress might be one of the causes of impaired endothelial functions resulting in myocardial ischaemia and chest pain in patients with CSX. The relatively preserved HDL and apolipoprotein-A1 levels in patients with CSX might be a protective mechanism against progression of coronary microvascular dysfunction to atherosclerotic coronary artery disease.

Demonstration of ventricular myocardial extensions into the pulmonary artery and aorta beyond the ventriculo-arterial junction.

BACKGROUND: A subgroup of outflow tract (OT) ventricular tachycardias (VT) originate from the aortic sinuses or the main stem of the pulmonary artery. The anatomic substrate for these tachycardias is unknown. The aim of this study was to investigate the presence of ventricular myocardial extensions (VME) into the pulmonary artery (PA) and aorta (Ao) beyond the ventriculo-arterial junction (VAJ) and determine the anatomical and histological characteristics of these muscle extensions. METHODS: Ninety-five consecutive human hearts obtained at autopsy were studied. Longitudinal strips of tissue containing each cusp, aortic, and pulmonary artery walls and left and right ventricular outflow tracts were excised and histologically analyzed. Anatomical measurements, including length and thickness of VMEs, obtained at autopsy, were made. RESULTS: VMEs beyond the VAJ were found in 21 of 95 (22%) patients studied. VMEs were found in 16 of 95 PAs (17%) and 7 of 95 Aos (7%) were examined. VMEs were located within the adventitia in 23 (88%) and on the epicardial surface in three (12%). The majority of VMEs were in continuity with the underlying ventricular OT muscle tissue. Myocellular hypertrophy and fibrosis were present in 19 (73%) and fatty tissue between the layers of VME in 18 (69%). Clinical data were available in 14 of 21 patients with positive VME. None of the patients (clinical data available group) had history of cardiac disease or signs or symptoms (palpitations or syncope) of cardiac disease. CONCLUSIONS: VMEs into the PA and Ao beyond the VAJ are relatively common. It seems that their mere presence does not predispose to OT VTs. There are probably intrinsic arrhythmogenic properties in tissues specific to these regions in those patients who develop OT VTs.

Acute myocardial infarction following an arthropod bite: is hereditary thrombophilia a contributing factor?

Acute myocardial infarction (AMI) due to arthropod envenomation has rarely been reported in the literature. In the present report, we describe two cases who developed AMI following an arthropod bite. Coronary angiograms revealed normal coronary arteries in both patients. Both events were probably secondary to coronary artery thrombosis and/or coronary artery vasospasm. Both patients were subsequently found to be heterozygous for prothrombin mutation (G20210A). As a result, we recommend ruling out the possibility of hereditary thrombophilias in young patients with AMI developing after an arthropod bite.

Homozygous factor V Leiden mutation in two siblings presenting with acute myocardial infarction: a rare cause of myocardial infarction in the young.

Although factor V Leiden mutation, is the most common established genetic risk factor for venous thrombosis, its effect on the development of myocardial infarction remains unclear. We describe a family case of homozygous factor V Leiden mutation in two siblings presenting with acute myocardial infarction as a rare cause of myocardial infarction in the young.