Prognostic value of mitral regurgitation assessment during exercise echocardiography in patients with left ventricular dysfunction: a follow-up study of 1.7 +/- 1.5 years.

AIMS: The value of exercise echocardiography (EE) over resting echocardiography when this last incorporates information on mitral regurgitation (MR) is only partially known. Furthermore, limited data exist regarding the value of MR worsening during exercise in patients with left ventricular (LV) dysfunction. We investigate whether EE has incremental value over a resting echo-Doppler study; and whether post-exercise MR increments the value of EE for predicting outcome in patients with LV dysfunction. METHODS AND RESULTS: Three hundred and twenty-three consecutive patients with LV dysfunction (LV ejection fraction < or =45%) referred for EE were followed for 1.7 +/- 1.5 years. There were 43 hard events (myocardial infarction in 9 and cardiac death in 34). Resting MR, peak heart rate x blood pressure, and number of involved territories at exercise were independently associated to hard events (incremental P-value of EE =0.02). Independent variables associated to cardiac death were resting MR, peak heart rate x blood pressure, peak wall motion score index, and MR worsening (incremental P-value of MR worsening = 0.04). CONCLUSIONS: EE maintains its prognostic value over resting echocardiography even when this last incorporates information on MR. Exercise-induced MR worsening has independent prognostic value for cardiac death in patients with LV dysfunction.

Major adverse events and atrial tachycardia in Ebstein's anomaly predicted by cardiovascular magnetic resonance.

OBJECTIVES: Patients with Ebstein's anomaly of the tricuspid valve (EA) are at risk of tachyarrhythmia, congestive heart failure and sudden cardiac death. We sought to determine the value of cardiovascular magnetic resonance (CMR) for predicting these outcomes. METHODS: Seventy-nine consecutive adult patients (aged 37±15 years) with unrepaired EA underwent CMR and were followed prospectively for a median 3.4 (range 0.4-10.9) years for clinical outcomes, namely major adverse cardiovascular events (MACEs: sustained ventricular tachycardia/heart failure hospital admission/cardiac transplantation/death) and first-onset atrial tachyarrhythmia (AT). RESULTS: CMR-derived variables associated with MACE (n=6) were right ventricular (RV) or left ventricular (LV) ejection fraction (EF) (HR 2.06, 95% CI 1.168 to 3.623, p=0.012 and HR 2.35, 95% CI 1.348 to 4.082, p=0.003, respectively), LV stroke volume index (HR 2.82, 95% CI 1.212 to 7.092, p=0.028) and cardiac index (HR 1.71, 95% CI 1.002 to 1.366, p=0.037); all remained significant when tested solely for mortality. History of AT (HR 11.16, 95% CI 1.30 to 95.81, p=0.028) and New York Heart Association class >2 (HR 7.66, 95% CI 1.54 to 38.20, p=0.013) were also associated with MACE; AT preceded all but one MACE, suggesting its potential role as an early marker of adverse outcome (p=0.011).CMR variables associated with first-onset AT (n=17; 21.5%) included RVEF (HR 1.55, 95% CI 1.103 to 2.160, p=0.011), total R/L volume index (HR 1.18, 95% CI 1.06 to 1.32, p=0.002), RV/LV end diastolic volume ratio (HR 1.55, 95% CI 1.14 to 2.10, p=0.005) and apical septal leaflet displacement/total LV septal length (HR 1.03, 95% CI 1.00 to 1.07, p=0.041); the latter two combined enhanced risk prediction (HR 6.12, 95% CI 1.67 to 22.56, p=0.007). CONCLUSION: CMR-derived indices carry prognostic information regarding MACE and first-onset AT among adults with unrepaired EA. CMR may be included in the periodic surveillance of these patients.

Relation of left ventricular chamber stiffness at rest to exercise capacity in hypertrophic cardiomyopathy.

The degree of exercise capacity is poorly predicted by conventional markers of disease severity in patients with hypertrophic cardiomyopathy (HC). The principal mechanism of exercise intolerance in patients with HC is the failure of stroke volume augmentation due to left ventricular (LV) diastolic dysfunction. The role of LV chamber stiffness, assessed noninvasively, as a determinant of exercise tolerance is unknown. Sixty-four patients with HC were studied with Doppler echocardiography, exercise testing, and gadolinium cardiac magnetic resonance. The LV chamber stiffness index was determined as the ratio of pulmonary capillary wedge pressure (derived from the E/Ea ratio) to LV end-diastolic volume (assessed by cardiac magnetic resonance). Maximal exercise tolerance was defined as achieved METs. There were inverse correlations between METs achieved and age (r = -0.38, p = 0.003), heart rate deficit (r = -0.39, p = 0.002), LV outflow tract gradient (r = -0.33, p = 0.009), the E/Ea ratio (r = -0.4, p = 0.001), mean LV wall thickness (r = -0.26, p = 0.04), and LV stiffness (r = -0.56, p <0.001) and a positive correlation between METs achieved and LV end-diastolic volume (r = 0.33, p = 0.01). On multivariate analysis, only LV chamber stiffness was associated with exercise capacity. A LV stiffness level of 0.18 mm Hg/ml had 100% sensitivity and 75% specificity (area under the curve 0.84) for predicting < or =7 METs achieved. In conclusion, LV diastolic dysfunction at rest, as manifested by increased LV chamber stiffness, is a major determinant of maximal exercise capacity in patients with HC.

Exercise intolerance in adult congenital heart disease: comparative severity, correlates, and prognostic implication.

BACKGROUND: Although some patients with adult congenital heart disease (ACHD) report limitations in exercise capacity, we hypothesized that depressed exercise capacity may be more widespread than superficially evident during clinical consultation and could be a means of assessing risk. METHODS AND RESULTS: Cardiopulmonary exercise testing was performed in 335 consecutive ACHD patients (age, 33+/-13 years), 40 non-congenital heart failure patients (age, 58+/-15 years), and 11 young (age, 29+/-5 years) and 12 older (age, 59+/-9 years) healthy subjects. Peak oxygen consumption (peak VO2) was reduced in ACHD patients compared with healthy subjects of similar age (21.7+/-8.5 versus 45.1+/-8.6; P<0.001). No significant difference in peak VO2 was found between ACHD and heart failure patients of corresponding NYHA class (P=NS for each NYHA class). Within ACHD subgroups, peak VO2 gradually declined from aortic coarctation (28.7+/-10.4) to Eisenmenger (11.5+/-3.6) patients (P<0.001). Multivariable correlates of peak VO2 were peak heart rate (r=0.33), forced expiratory volume (r=0.33), pulmonary hypertension (r=-0.26), gender (r=-0.23), and body mass index (r=-0.19). After a median follow-up of 10 months, 62 patients (18.5%) were hospitalized or had died. On multivariable Cox analysis, peak VO2 predicted hospitalization or death (hazard ratio, 0.937; P=0.01) and was related to the frequency and duration of hospitalization (P=0.01 for each). CONCLUSIONS: Exercise capacity is depressed in ACHD patients (even in allegedly asymptomatic patients) on a par with chronic heart failure subjects. Lack of heart rate response to exercise, pulmonary arterial hypertension, and impaired pulmonary function are important correlates of exercise capacity, as is underlying cardiac anatomy. Poor exercise capacity identifies ACHD patients at risk for hospitalization or death.

[Beta-myosin heavy-chain gene mutations in patients with hypertrophic cardiomyopathy]. / Mutaciones en el gen de la cadena pesada de la betamiosina en pacientes con miocardiopatía hipertrófica.

INTRODUCTION AND OBJECTIVES: To determine the frequency of mutations in the beta-myosin heavy-chain gene (MYH7) in a cohort of patients with hypertrophic cardiomyopathy (HCM) and their families, and to investigate correlations between genotype and phenotype. METHODS: Single-strand conformation polymorphism analysis and sequencing of fragments with abnormal MYH7 gene mobility were carried out in 128 consecutive index patients with HCM. The phenotypes of patients with and without mutations were compared and the phenotypes of identified families were recorded. RESULTS: A total of 11 mutations were found in 13 families (10%); 7/11 had been previously described. The I736T mutation was found in three families and the A797T in two. One patient had two mutations (i.e., I736T and R787H). Mutations were more frequent in patients with a family history of sudden death (31%) and in those with severe hypertrophy (39% had a thickness > or = 30 mm). Mutations were found in 29 of 42 members of the 13 families, including six family members (20%) who were healthy carriers and aged < or = 36 years. Sudden death had occurred in eight members of four families: four in two families with the I736T mutation, one in a family with A797T, one in a family with R870H, and two in a family with A901P. CONCLUSIONS: MYH7 mutations were present in 10% of our families. Mutations were more frequent in patients with a family history of sudden death and in those with severe hypertrophy. Most mutations had been described previously. Some appeared in several families. For some mutations, the correlation between genotype and phenotype was stable, while for others, there were marked differences between the phenotypes of the index patients and their relatives, suggesting the presence of additional genetic factors that have yet to be identified.

[Pulmonary arterial hypertension in adults with congenital heart disease]. / Hipertensión arterial pulmonar en adultos con cardiopatía congénita.

Pulmonary arterial hypertension is a chronic, persistent elevation in pulmonary artery pressure without evidence of left heart failure. Pulmonary hypertension is common in patients with adult congenital heart disease and is usually the result of an increase of pulmonary blood flow through a large left to right shunt. This condition is progressive and patients are symptomatic and usually die between the third and fifth decades of life. To date, there is no standardized treatment for this condition and a general policy of non-intervention to avoid destabilization of the balanced physiology is recommended. Intravenous prostanoids have been shown to have an effect but they are invasive and associated with major side effects. Lung and combined heart and lung transplantation might be a therapeutic option for selected patients. However, donor shortage is a major issue. Oral advanced therapies have been recently shown to improve haemodynamics and survival in idiopathic pulmonary hypertension or in pulmonary hypertension related to scleroderma and may have a role in patients with pulmonary hypertension secondary to congenital heart disease.

Familial dilated cardiomyopathy and isolated left ventricular noncompaction associated with lamin A/C gene mutations.

LMNA mutations have been associated with familial or sporadic dilated cardiomyopathy (DC), with or without conduction system disease. We studied the LMNA gene in 67 consecutive patients with DC (18 had familial DC, 17 had possible familial DC, and 32 sporadic DC). From genomic DNA, coding regions of the LMNA gene were amplified by polymerase chain reaction, studied by single-strand conformation polymorphism, and cycle sequenced. Mutations were confirmed by restriction fragment length polymorphism. Two disease-causing mutations were found in families A and B. In family A, a novel R349L mutation was present in the mother and her identical twin daughters. They required cardiac transplantation at 36, 18, and 20 years of age. In family B, the R190W mutation was present in 2 cousins with DC and without conduction system disease (1 had cardiac transplantation at 45 years of age and 1 died suddenly at 46 years of age) and in 2 of their sons. The mothers of the 2 affected patients died due to cardiac causes in their 40s (1 died suddenly). One of the carriers fulfilled diagnostic criteria for isolated left ventricular noncompaction. Our data associated the R349L and R190W mutations in LMNA with severe forms of familial DC. LMNA mutations should be considered in the genetic screening of patients with familial DC without conduction system disease. Isolated left ventricular noncompaction may be part of the phenotypic spectrum of the laminopathies.

[Familial dilated cardiomyopathy in patients transplanted for idiopathic dilated cardiomyopathy]. / Miocardiopatía dilatada familiar en pacientes trasplantados por miocardiopatía dilatada idiopática.

OBJECTIVE: To evaluate the prevalence, clinical features, and pattern of inheritance of familial dilated cardiomyopathy (DCM) in heart transplant patients. PATIENTS AND METHOD: Patients with idiopathic DCM who had undergone heart transplantation were invited to participate. Patients with alcohol abuse were excluded. A clinical evaluation, 12-lead ECG, echocardiogram, blood tests, and DNA extraction were performed in patients and relatives. Familial DCM was defined as the presence of at least one relative with idiopathic DCM. Possible familial DCM was considered when at least one relative had left ventricular enlargement (LVE) (> 112% predicted LVEDD). RESULTS: One hundred and ninety-nine relatives of 43 families were studied. DCM was familial in 11 probands (25.6%) and possibly familial in 11 (25.6%). Fifteen relatives had DCM (7.5%), 26 (13.1%) LVE, and 5 (2.5%) hypertrophic cardiomyopathy. The pattern of inheritance was autosomal dominant in most families. Five probands (3 with familial DCM) had antecedents of consanguinity and possible recessive inheritance. Six probands (14%, 1 with familial DCM) had relatives with conduction system defects. Creatine kinase was moderately increased in 9 relatives (4.5%), 3 of them with LVE. Fifteen patients had at least moderate alcohol intake. Three of them had familial DCM (relatives without alcohol abuse) and 6 had possible familial DCM. CONCLUSIONS: The prevalence of familial DCM is high in patients who undergo heart transplant. Left ventricular enlargement, conduction system abnormalities, and elevated creatine kinase may be early markers of familial disease. Hypertrophic cardiomyopathy is present in some relatives of patients with idiopathic DCM. Familial DCM is present in patients with a previous diagnosis of alcoholic DCM.

The shape and function of the right ventricle in Ebstein's anomaly.

BACKGROUND: Ebstein's anomaly involves both the right ventricle (RV) and tricuspid valve. METHODS: The functional RV and tricuspid orifice were traced from magnetic resonance images in 29 adult Ebstein patients and 9 normal subjects and reconstructed for visualization and measurement of regional RV size, function, and shape at 20 cross sections, and inlet and outflow tract ejection fractions (EFs). RESULTS: The RV in Ebstein's had RV dilation (end diastolic volume index 179 ± 69 vs. 84 ± 22 ml/m(2) in normals, p<0.001) and global dysfunction (EF 45 ± 8 vs. 55 ± 5% in normals, p<0.001). Longitudinal contraction was preserved (26 ± 13 vs. 26 ± 4 mm in normals) and correlated more weakly with EF than short axis fractional shortening (r=0.44 vs. r=0.71, p<0.05 for both). The apical region in Ebstein's RV was enlarged, rounded and contributed more than normal to the global stroke volume. However this contribution correlated inversely with global EF. In contrast slices in the basal region had normal cross sectional area and their function correlated directly with global EF. Inlet EF was depressed (46 ± 8% vs. 55 ± 6 in normals, p=.002); outflow tract EF was even more depressed (39 ± 14, p=0.019). CONCLUSION: The three dimensional shape of the RV in adult Ebstein patients was demonstrated. The Ebstein's RV remodels in diverse regional patterns rather than following a shape continuum. Changes at the apex and base had opposing effects on function. Global EF was supported more by short axis than longitudinal contraction.

Prognostic value of exercise echocardiography in patients with left bundle branch block.

OBJECTIVES: Our aim was to evaluate the role of exercise echocardiography for predicting outcome in a cohort of patients with left bundle branch block (LBBB). BACKGROUND: Although the prognostic value of exercise echocardiography has been well established in several subgroups of patients, it has not been specifically assessed in patients with LBBB. METHODS: Of the 8,050 patients who underwent treadmill exercise echocardiography, 618 demonstrated complete LBBB. Nine patients were lost to follow-up and 609 patients were included in this study. Wall motion score index (WMSI) was evaluated at rest and at peak exercise, and the difference (DeltaWMSI) was calculated. Ischemia was defined as the development of new or worsening wall motion abnormalities with exercise. End points were all-cause mortality and major cardiac events (including cardiac death, myocardial infarction, or cardiac transplantation). Mean follow-up was 4.6 +/- 3.4 years. RESULTS: Mean age was 66 +/- 10 years, and 331 patients (54%) were men. A total of 177 patients (29%) developed ischemia with exercise. During follow-up, 124 deaths occurred, and 74 patients had a major cardiac event before any revascularization procedure. Patients with ischemia had a greater 5-year mortality rate (24.6% vs. 12.6%, p < 0.001) and 5-year major cardiac events rate (18.1% vs. 9.7%, p = 0.003). In multivariate analysis, DeltaWMSI remained an independent predictor of mortality (hazard ratio: 2.42, 95% confidence interval: 1.21 to 4.82, p = 0.012) and major cardiac events (hazard ratio: 3.38, 95% confidence interval: 1.30 to 8.82, p = 0.013). Exercise echocardiographic results also provided incremental value over clinical, resting echocardiographic, and treadmill exercise data for the prediction of mortality (p = 0.014) and major cardiac events (p = 0.017). CONCLUSIONS: Exercise echocardiography provides significant prognostic information for predicting outcome in patients with LBBB. As compared to patients with normal exercise echocardiograms, patients with abnormal results are at increased risk of mortality and major cardiac events.

[Reconstruction of the right ventricular outflow tract using a Medtronic Freestyle aortic root bioprosthesis]. / Reconstrucción del tracto de salida del ventrículo derecho con raíz aórtica protésica Medtronic Freestyle.

Uncorrected, long-term pulmonary regurgitation leads to right ventricular dilatation and dysfunction in a significant percentage of patients. We used magnetic resonance imaging (MRI) before and after surgery to assess the effect of pulmonary valve replacement with the Medtronic Freestyle bioprosthesis on right ventricular function and volume in nine patients with pulmonary regurgitation or stenosis. Mean follow-up time was 26 (10) months. We observed a decrease in mean end-diastolic volume from 143.6 (85.1) mL/m2 to 74.1 (12.6) mL/m2 (P=.018) and, in end-systolic volume from 88.0 (50.3) mL/m2 to 35.8 (19.3) mL/m2 (P=.016). In pulmonary valve disease, extensive follow-up by MRI is essential for timely evaluation of the degree of right ventricular dilation or dysfunction and for selecting a suitable time for valve replacement. The Medtronic Freestyle bioprosthesis is a good surgical choice for pulmonary valve replacement as its use is associated with low morbidity and mortality and the successful normalization of ventricular volumes.

Risk stratification by treadmill exercise echocardiography in patients with excellent exercise capacity.

BACKGROUND: The incremental value of exercise echocardiography (EE) has been demonstrated to be maximal in patients with moderate pretest probability for coronary artery disease, but there is a lack of data in patients with low pretest probability or patients with good functional capacity. METHODS: To investigate whether such incremental value is maintained in patients with excellent exercise capacity, we studied 1,433 patients who had excellent exercise capacity (>or=8 METs for women, >or=10 METs for men). RESULTS: During a follow-up of 2.3 +/- 1.5 years, 42 hard events occurred (cardiac death or nonfatal myocardial infarction). Variables independently associated to hard events were male gender (P = 0.04), % of the age-predicted maximum heart rate (P = 0.02), chronotropic reserve (P = 0.002), and abnormal EE (P = 0.03; incremental P value of EE = 0.03). CONCLUSIONS: EE has incremental value over clinical variables, resting echocardiography, and exercise testing variables in patients with excellent exercise capacity. EE may be preferable to ECG exercise testing even in patients expected to have good exercise capacity.

[Clinical significance of late gadolinium enhancement on cardiovascular magnetic resonance in patients with hypertrophic cardiomyopathy]. / Significado clínico del realce tardío de gadolinio con resonancia magnética en pacientes con miocardiopatía hipertrófica.

INTRODUCTION AND OBJECTIVES: In patients with hypertrophic cardiomyopathy, myocardial fibrosis can be detected by late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging. We investigated the relationships between the extent of LGE, left ventricular morphology and function, and clinical characteristics. METHODS: Both cine and gadolinium-enhanced magnetic resonance imaging were performed in 104 patients with hypertrophic cardiomyopathy. RESULTS: Fifty patients (48%) showed LGE (range: 1-11 segments). The extent of LGE was positively correlated with maximum left ventricular wall thickness (r=0.53, P< .001), left ventricular mass (r=0.41, P< .001), and the number of hypokinetic segments (r=0.51, P< .001), and inversely correlated with ejection fraction (r=-0.32, P=.001), the magnitude of the subaortic gradient increase during exercise echocardiography (r=-0.26, P=.023), and age at diagnosis (r=-0.20, P=.04). Four of the five patients with an ischemic response on exercise echocardiography had > or =3 segments showing LGE (P=.003). Severe hypertrophy (i.e., > or =30 mm) and nonsustained ventricular tachycardia occurred more frequently as the number of LGE segments increased (P< .001 and P=.04, respectively). CONCLUSIONS: Extensive LGE reflects greater disease expression. It is associated with more severe myocardial damage (i.e., a lower ejection fraction and a larger number of hypokinetic segments) and with adverse clinical characteristics (e.g., young age at diagnosis, severe hypertrophy, nonsustained ventricular tachycardia, and an ischemic response on exercise), suggesting that it may be closely linked to prognosis.

[Value of resting and exercise mitral regurgitation during exercise echocardiography to predict outcome in patients with left ventricular dysfunction]. / Valor pronóstico de la regurgitación mitral en reposo y ejercicio durante la ecocardiografía de ejercicio en pacientes con disfunción ventricular izquierda.

INTRODUCTION AND OBJECTIVES: The relative value of exercise echocardiography (EE) over resting echocardiography when this last incorporates information on mitral regurgitation (MR) is unknown. Furthermore, limited data exists regarding to the value of MR worsening during exercise in patients with LV dysfunction. We investigated whether: a) EE has incremental value over a resting echo-Doppler study; and b) post-exercise MR increments the value of EE for predicting outcome in patients with LV dysfunction. METHODS: 388 consecutive patients with LV dysfunction (LV ejection fraction <50%) were followed for 2.1 (1.5) years. There were 46 hard events (myocardial infarction in 10 and cardiac death in 36). RESULTS: There were 43 events in 319 patients with abnormal EE vs 3 events in 69 patients with normal EE (13% vs 4%, P=.04), whereas there were 20 events in the 103 patients with at least moderate resting MR vs 26 events in the 288 with no/mild MR (19% vs 9%, P=.006). Resting MR, peak heart rate x blood pressure, and n masculine of diseased territories on EE were independently associated to hard events. The same variables and MR worsening were independently associated to cardiac death. CONCLUSIONS: EE maintains its higher prognostic value over resting echocardiography even when this last incorporates information on MR. MR worsening increments the value of EE for predicting cardiac death in patients with LV dysfunction.

Pulmonary arterial thrombosis in eisenmenger syndrome is associated with biventricular dysfunction and decreased pulmonary flow velocity.

OBJECTIVES: This study sought to determine what factors are associated with pulmonary artery thrombi in Eisenmenger patients. BACKGROUND: Pulmonary artery thrombosis is common in Eisenmenger syndrome, although its underlying pathophysiology is poorly understood. METHODS: Adult patients with Eisenmenger syndrome underwent computed tomography pulmonary angiography, cardiac magnetic resonance imaging, and echocardiography. Measurement of ventricular function, pulmonary artery size, and pulmonary artery blood flow were obtained. Hypercoagulability screening and platelet function assays were performed. RESULTS: Of 55 consecutive patients, 11 (20%) had a detectable thrombus. These patients were older (p = 0.032), but did not differ in oxygen saturation, hemoglobin, or hematocrit from those without thrombus. Right ventricular ejection fraction by magnetic resonance imaging was lower in those with thrombus (0.41 +/- 0.15 vs. 0.53 +/- 0.13, p = 0.017), as was left ventricular ejection fraction (0.48 +/- 0.12 vs. 0.60 +/- 0.09, p = 0.002), a finding corroborated by tissue Doppler and increased brain natriuretic peptide. Those with thrombus also had a larger main pulmonary artery diameter (48 +/- 14 mm vs. 38 +/- 9 mm, p = 0.007) and a lower peak systolic velocity in the pulmonary artery (p = 0.003). There were no differences in clotting factors, platelet function, or bronchial arteries between groups. Logistic regression showed pulmonary artery velocity to be independently associated with thrombosis. CONCLUSIONS: Pulmonary arterial thrombosis among adults with Eisenmenger syndrome is common and relates to older age, biventricular dysfunction, and slow pulmonary artery blood flow rather than degree of cyanosis or coagulation abnormalities. Further work to define treatment efficacy is needed.

Risk stratification by treadmill exercise echocardiography.

BACKGROUND: Although exercise echocardiography (EE) has value for the diagnosis of coronary artery disease (CAD), it's not clear whether it may be useful for risk assessment in all categories of patients. To determine whether: 1) there is an incremental value of EE over clinical, exercise and resting echocardiographic variables for the prediction of events according to the pre-test probability of CAD; and 2) the number, location of the diseased territories, and nature of the disease affect the risk stratification, we studied 2436 patients referred for EE that were followed for 2.1 +/- 1.5 years. METHODS: Based on a pre-test score, previous myocardial infarction (MI) or revascularizations, 1242 patients were considered as having high, 1038 moderate, and 156 low pre-test probability. RESULTS: There were 89 hard events (myocardial infarction or cardiovascular death) in the 1203 patients with abnormal EE vs. 31 events in the 1233 with normal EE (p < 0.0001). Gender, Mets, heart rate x blood pressure, resting wall motion score index and number of involved territories at exercise were independently associated to hard events (final Chi-square = 170, incremental p value of exercise echo <0.0001). The incremental value of exercise echo over other variables was found in patients with the different pre-test probabilities. CONCLUSIONS: Exercise echocardiography has incremental value over clinical, exercise and resting echocardiographic variables in patients with different pre-test probabilities of CAD.

Interpretation of electrocardiographic abnormalities in hypertrophic cardiomyopathy with cardiac magnetic resonance.

AIMS: To clarify the mechanisms of electrocardiographic abnormalities in hypertrophic cardiomyopathy, 102 patients were examined with cardiac magnetic resonance. Distribution and magnitude of hypertrophy and late-enhancement were correlated with electrocardiographic abnormalities. METHODS AND RESULTS: Abnormal Q waves were associated with greater upper anterior septal thickness (22+/-7 mm vs. 18+/-5 mm, P=0.001) and increased ratios of upper anterior septum to mean inferolateral (P=0.01), anterolateral (P=0.002), apical (P=0.001), and right ventricular (P=0.001) wall thickness. There was no relation between abnormal Q waves and late-enhancement, except for Q waves >/=40 ms (P=0.02). Conduction disturbances and absent septal Q waves were associated with late-enhancement (89 vs. 45%, P=0.01 and 75 vs. 39%, P=0.002, respectively). The depth of negative T waves was related to an increased ratio of the mean thickness between apical and basal level (P=0.01), and to the presence of apical late-enhancement (P=0.03). CONCLUSION: Abnormal Q waves reflect the interrelation between upper anterior septal thickness and other regions of the left and right ventricles, and wider Q waves are associated with late-enhancement. Conduction disturbances and absent septal Q waves are associated with late-enhancement. The depth of negative T waves is related to craniocaudal asymmetry and apical late-enhancement.