Diagnostic approach to assessment of valvular heart disease using MRI-Part I: a practical approach for valvular regurgitation.

Valvular heart diseases from any cause are divided into two categories: stenosis and regurgitation. Acquired knowledge of the pathological aetiology and disease severity are the important clues for optimal treatment, which may be medication or combination with surgery. The non-invasive techniques have been established for valvular heart disease evaluation for many years especially in demonstrating valvular structure and assessing severity. Transthoracic echocardiography still plays the major role. However, not every case can be clearly evaluated by transthoracic echocardiography because of rib space window limitation. In the present-day practice, MRI has been extensively used for the evaluation of heart diseases in both unique and complementary categories. However, valvular heart disease assessment using cardiac MRI still remains an important challenge.

Diagnostic approach to assessment of valvular heart disease using magnetic resonance imaging, part II: a practical approach for native and prosthetic heart valve stenosis.

MRI is already an established diagnostic modality for assessing valvular stenosis although it is not usually used as the initial non-invasive test. The preferred diagnostic modality for valvular stenosis is currently echocardiography. However, MRI has been offered as a good alternative test in the event of inconclusive echocardiography results. During the course of valvular stenosis, the valve orifice area decreases and the pressure gradient across the diseased valve increases. Valvular orifice area is the major core indicator for valvular stenosis severity grading. Compared with valvular regurgitation, assessment with MRI for valvular stenosis is less complicated. The aim of this article is to detail the MRI techniques in assessing native and prosthetic heart valve stenosis.

Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium.

BACKGROUND: The underlying electrophysiological mechanism that causes an abnormal ECG pattern and ventricular tachycardia/ventricular fibrillation (Vt/VF) in patients with the Brugada syndrome (BrS) remains unelucidated. However, several studies have indicated that the right ventricular outflow tract (RVOT) is likely to be the site of electrophysiological substrate. We hypothesized that in patients with BrS who have frequent recurrent VF episodes, the substrate site is the RVOT, either over the epicardium or endocardium; abnormal electrograms would be identified at this location, which would serve as the target site for catheter ablation. METHODS AND RESULTS: We studied 9 symptomatic patients with the BrS (all men; median age 38 years) who had recurrent VF episodes (median 4 episodes) per month, necessitating implantable cardioverter defibrillator discharge. Electroanatomic mapping of the right ventricle, both endocardially and epicardially, and epicardial mapping of the left ventricle were performed in all patients during sinus rhythm. All patients had typical type 1 Brugada ECG pattern and inducible Vt/VF; they were found to have unique abnormal low voltage (0.94±0.79 mV), prolonged duration (132±48 ms), and fractionated late potentials (96±47 ms beyond QRS complex) clustering exclusively in the anterior aspect of the RVOT epicardium. Ablation at these sites rendered Vt/VF noninducible (7 of 9 patients [78%]; 95% confidence interval, 0.40 to 0.97, P=0.015) and normalization of the Brugada ECG pattern in 89% (95% confidence interval, 0.52 to 0.99; P=0.008). Long-term outcomes (20±6 months) were excellent, with no recurrent Vt/VF in all patients off medication (except 1 patient on amiodarone). CONCLUSIONS: The underlying electrophysiological mechanism in patients with BrS is delayed depolarization over the anterior aspect of the RVOT epicardium. Catheter ablation over this abnormal area results in normalization of the Brugada ECG pattern and prevents Vt/VF, both during electrophysiological studies as well as spontaneous recurrent Vt/VF episodes in patients with BrS.

Differential effects of progenitor cell populations on left ventricular remodeling and myocardial neovascularization after myocardial infarction.

OBJECTIVES: We compared biological repair after acute myocardial infarction (AMI) with selected porcine progenitor cell populations. BACKGROUND: Cell types and mechanisms responsible for myocardial repair after AMI remain uncertain. METHODS: In a blinded, randomized study, we infused autologous late-outgrowth endothelial progenitor cells (EPC) (n = 10, 34 +/- 22 x 10(6) CD29-31-positive, capable of tube formation), allogeneic green fluorescent peptide-labeled mesenchymal stem cells (MSC) (n = 11, 10 +/- 2 x 10(6) CD29-44-90-positive, capable of adipogenic and osteogenic differentiation), or vehicle (CON) (n = 12) in the circumflex artery 1 week after AMI. Systolic function (ejection fraction), left ventricular (LV) end-diastolic and end-systolic volumes, and infarct size were assessed with magnetic resonance imaging at 1 week and 7 weeks. Cell engraftment and vascular density were evaluated on postmortem sections. RESULTS: Recovery of LV ejection fraction from 1 to 7 weeks was similar between groups, but LV remodeling markedly differed with a greater increase of LV end-systolic volume in MSC and CON (+11 +/- 12 ml/m(2) and +7 +/- 8 ml/m(2) vs. -3 +/- 11 ml/m(2) in EPC, respectively, p = 0.04), and a similar trend was noted for LV end-diastolic volume (p = 0.09). After EPC, infarct size decreased more in segments with >50% infarct transmurality (p = 0.02 vs. MSC and CON) and was associated with a greater vascular density (p = 0.01). Late outgrowth EPCs secrete higher levels of the pro-angiogenic placental growth factor (733 [277 to 1,214] pg/10(6) vs. 59 [34 to 88] pg/10(6) cells in MSC, p = 0.03) and incorporate in neovessels in vivo. CONCLUSIONS: Infusion of late-outgrowth EPCs after AMI improves myocardial infarction remodeling via enhanced neovascularization but does not mediate cardiomyogenesis. Endothelial progenitor cell transfer might hold promise for heart failure prevention via pro-angiogenic or paracrine matrix-modulating effects.

Improvement in the severity of mitral regurgitation after direct intramyocardial injection of angiogenic cell precursor.

We reported a case of dilated cardiomyopathy and moderate-severe mitral regurgitation (MR) who we treated by surgical direct intramyocardial angiogenic cell precursors injection. The patient was a New York Heart Association functional class III-IV, 56 year old man, who presented with end-stage congestive heart failure, moderate/severe mitral regurgitation, and myocardial fibrosis with the left ventricular ejection fraction of 13%. After he underwent direct surgical intramyocardial cell implantation, the myocardial fibrosis was resolved at 3 months follow-up. The severity of MR reduced to moderate and mild at 3 and 9 months, respectively. The left ventricular function gradually improved up to 53% at 19 months. To our knowledge, this is one of the only reports of successful direct surgical intramyocardial peripheral blood stem cell implantation to treat MR in dilated cardiomyopathy patient.

Time course of reversed cardiac remodeling after pulmonary endarterectomy in patients with chronic pulmonary thromboembolism.

To evaluate the time course of reversed remodeling after pulmonary endarterectomy (PEA) in patients with chronic thromboembolic pulmonary hypertension(CTPEH), we studied 22 patients (age: 60 +/- 13 years) with MRI immediately before, 1 month, 3 months, and 6 months after PEA. MRI included assessment of biventricular function, aortic and pulmonary artery(PA) flow, and right ventricular (RV) overload using the ratio of RV-to-biventricular diameter. Except in one patient, who died 2 months post-surgery, clinical improvement occurred early after PEA (NYHA class: 3.3 +/- 0.6 to 1.5 +/- 0.8, p < 0.0001) with a decrease of systolic pulmonary artery pressures (79 +/- 14 to 44 +/- 14 mmHg, p < 0.0001). At 1 month post PEA, RV end-diastolic volumes decreased (198 +/- 72 to 137 +/- 59 ml, p < 0.0001), and the RV ejection fraction (EF) improved (31 +/- 9 to 47 +/- 10%, p < 0.0001). No further significant improvement in pulmonary pressures or RV function occurred at 3 months or 6 months. Although no significant change was found in LV volumes or function, aortic flow increased early after surgery. PEA had only a beneficial effect on right PA flow. RV overload decreased early after PEA (ratio RV-to-biventricular diameter: before: 0.67 +/- 0.04, after: 0.54 +/- 0.06, p < 0.0001), showing a good correlation with the improvement in RVEF (r = 0.7, P < 0.0001). In conclusion, reversed cardiac remodeling occurs early after PEA, to slow down after 1 month. At 6 months, cardiac remodeling is incomplete as witnessed by low-normal RV function and residually elevated PA pressures.

Defibrillator Versus beta-Blockers for Unexplained Death in Thailand (DEBUT): a randomized clinical trial.

BACKGROUND: Sudden Unexplained Death Syndrome (SUDS) is the leading cause of death in young, healthy, Southeast Asian men. The role of an implantable cardioverter defibrillator (ICD) for mortality reduction in these patients remains unclear. METHODS AND RESULTS: The Defibrillator Versus beta-Blockers for Unexplained Death in Thailand (DEBUT) study is a randomized, clinical trial conducted in 2 phases (pilot study followed by the main trial) to compare the annual all-cause mortality rates among SUDS patients treated with beta-blockers versus that among those treated with an ICD. A total of 86 patients who were SUDS survivors and probable SUDS survivors were randomized to receive an ICD or propranolol (20 patients were in the pilot study and 66 were in the main trial). The primary end point was death from all causes. The secondary end point was recurrent ventricular tachycardia/ventricular fibrillation (VF) or cardiac arrest. During the 3-year follow-up period of the main trial, there were 4 deaths; all occurred in the beta-blocker group (P=0.02). Seven subjects in the ICD arm had recurrent VF, and all were effectively treated by the ICD. On the basis of the main trial results, the Data Safety Monitoring Board stopped the study. In total (both from the Pilot study and the main trial), there were 7 deaths (18%) in the beta-blocker group and no deaths in the ICD group, but there were a total of 12 ICD patients receiving ICD discharges due to recurrent VF. CONCLUSIONS: ICD treatment provides full protection from death related to primary VF in a SUDS population and is superior to beta-blockade treatment.