Early Experience of Patients with left Bundle Branch Block Corrected through Left Bundle Branch Area Pacing Compared with Conventional Right Ventricular Pacing: A Single-Center Retrospective Study.

Background: Left bundle branch area pacing (LBBAP) has the advantages of narrow QRS duration, rapid peak left ventricular (LV) activation, and LV dyssynchrony correction with a low, stable pacing output. Here we report our experience with patients undergoing LBBAP with a left bundle branch block (LBBB) for clinically indicated pacemaker or cardiac resynchronization therapy implantation. We compared the initial follow-up data of these patients and patients undergoing conventional right ventricular pacing (RVP). Methods: This retrospective study was performed between January 2017 and December 2020 and recruited 19 consecutive patients (mean age: 63 years; 8 women, 11 men) who underwent LBBAP (13 LBBAP only and 6 LBBAP + LV pacing), and 14 consecutive patients (mean age: 75 years; 8 women, 6 men) who underwent RVP. Demographic data, QRS durations, and echocardiographic parameters were compared before and after the procedures. Results: LBBAP substantially shortened the QRS duration and improved LV dyssynchrony echocardiographic parameters. However, RVP was not significantly associated with prolonged QRS duration and worse LV dyssynchronization. LBBAP improved cardiac contractility in selected patients. We did not find adverse effects of LBBAP on patients with preserved systolic function, possibly due to the limited number of patients and follow-up time. However, two of the 11 patients with preserved systolic function at baseline who underwent conventional RVP developed heart failure after implantation. Conclusions: In our experience, LBBAP improves LBBB-related ventricular dyssynchrony. However, LBBAP requires greater skill, and doubts remain about lead extraction. LBBAP may be an option for patients with LBBB when performed by an experienced operator, however further studies are needed to verify our findings.

Estrogen and/or Estrogen Receptor α Inhibits BNIP3-Induced Apoptosis and Autophagy in H9c2 Cardiomyoblast Cells.

The process of autophagy in heart cells maintains homeostasis during cellular stress such as hypoxia by removing aggregated proteins and damaged organelles and thereby protects the heart during the times of starvation and ischemia. However, autophagy can lead to substantial cell death under certain circumstances. BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), a hypoxia-induced marker, has been shown to induce both autophagy and apoptosis. A BNIP3-docked organelle, e.g., mitochondria, also determines whether autophagy or apoptosis will take place. Estrogen (E2) and estrogen receptor (ER) alpha (ERα) have been shown to protect the heart against mitochondria-dependent apoptosis. The aim of the present study is to investigate the mechanisms by which ERα regulates BNIP3-induced apoptosis and autophagy, which is associated with hypoxic injury, in cardiomyoblast cells. An in vitro model to mimic hypoxic injury in the heart by engineering H9c2 cardiomyoblast cells to overexpress BNIP3 was established. Further, the effects of E2 and ERα in BNIP3-induced apoptosis and autophagy were determined in BNIP3 expressing H9c2 cells. Results from TUNEL assay and Immunoflourecense assay for LC3 puncta formation, respectively, revealed that ERα/E2 suppresses BNIP3-induced apoptosis and autophagy. The Western blot analysis showed ERα/E2 decreases the protein levels of caspase 3 (apoptotic marker), Atg5, and LC3-II (autophagic markers). Co-immunoprecipitation of BNIP3 and immunoblotting of Bcl-2 and Rheb showed that ERα reduced the interaction between BNIP3 and Bcl-2 or Rheb. The results confirm that ERα binds to BNIP3 causing a reduction in the levels of functional BNIP3 and thereby inhibits cellular apoptosis and autophagy. In addition, ERα attenuated the activity of the BNIP3 promoter by binding to SP-1 or NFκB sites.

Safety profile and utility of treadmill exercise in patients with high-gradient hypertrophic cardiomyopathy.

BACKGROUND: Exercise echocardiography in the evaluation of hypertrophic cardiomyopathy (HCM) provides valuable information for risk stratification, selection of optimal treatment, and prognostication. However, HCM patients with left ventricular outflow tract gradients ≥30mm Hg are often excluded from exercise testing because of safety considerations. We examined the safety and utility of exercise testing in patients with high-gradient HCM. METHODS: We evaluated clinical characteristics, hemodynamics, and imaging variables in 499 consecutive patients with HCM who performed 959 exercise tests. Patients were divided based on peak left ventricular outflow tract gradients using a 30-mm Hg threshold into the following: obstructive (n=152), labile-obstructive (n=178), and nonobstructive (n=169) groups. RESULTS: There were no deaths during exercise testing. We noted 20 complications (2.1% of tests) including 3 serious ventricular arrhythmias (0.3% of tests). There was no difference in complication rate between groups. Patients with obstructive HCM had a higher frequency of abnormal blood pressure response (obstructive: 53% vs labile: obstructive: 41% and nonobstructive: 37%; P=.008). Obstructive patients also displayed a lower work capacity (obstructive: 8.4±3.4 vs labile obstructive: 10.9±4.2 and nonobstructive: 10.2±4.0, metabolic equivalent; P<.001). Exercise testing provided incremental information regarding sudden cardiac death risk in 19% of patients with high-gradient HCM, and we found a poor correlation between patient-reported functional class and work capacity. CONCLUSION: Our results suggest that exercise testing in HCM is safe, and serious adverse events are rare. Although numbers are limited, exercise testing in high-gradient HCM appears to confer no significant additional safety hazard in our selected cohort and could potentially provide valuable information.

Impact of Prolonged Door-to-Balloon Times on the Diastolic Function in Acute ST-Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention.

BACKGROUND: Emerging evidence indicates that diastolic left ventricular (LV) function is a powerful outcome predictor after acute ST-elevation myocardial infarction (STEMI). We hypothesized that shorter door-to-balloon (D2B) times with early restoration of coronary perfusion may preserve diastolic LV function in STEMI patients undergoing primary percutaneous coronary intervention (PPCI). METHODS: This study enrolled 340 consecutive STEMI patients who underwent PPCI with D2B times of < 90 min in 232 patients and D2B times ≥ 90 min in 108 patients, who all received subsequent echocardiographic examination within 48 hours of hospitalization. RESULTS: Although the LV ejection fraction was similar (50.92% vs. 51.66%, p = 0.573), the proportion of E/E' ratio > 15 was greater in patients with D2B times ≥ 90 min compared to those with D2B times < 90 min (44.4% vs. 30.6%, p = 0.013). Logistic regression analysis revealed that D2B time ≥ 90 min [odds ratio (OR): 1.82, 95% confidence interval (Cl): 1.04-3.17, p = 0.035] was an independent predictor for LV diastolic dysfunction. The effect was more prominent in patients ≥ 65 years of age (OR: 2.77, 95% CI: 1.09-7.00, p = 0.032), in whom the fraction of LV diastolic dysfunction increased proportionally with prolonged D2B times. CONCLUSIONS: Prolonged D2B time of greater than 90 min predicted LV diastolic dysfunction, particularly in aged subjects. D2B times shortening is important to preserve diastolic heart function after PPCI. KEY WORDS: Acute myocardial infarction; Diastolic dysfunction; Door-to-balloon time; Primary percutaneous coronary intervention.

Precordial ST-Segment Elevation Caused by Proximal Occlusion of a Non-Dominant Right Coronary Artery.

UNLABELLED: For patients with ST-segment elevation myocardial infarction, primary percutaneous coronary intervention to the culprit lesion via electrocardiographic guidance is essential. We herein report the rare case of a 49-year-old man who presented with ST-segment elevation in the precordial leads, while coronary angiography results indicated total occlusion of the proximal non-dominant right coronary artery. We evaluated its possible pathophysiologic mechanisms and thoroughly discussed isolated right ventricular infarction and its electrocardiography findings. KEY WORDS: Coronary angiography; Myocardial infarction; Total occlusions.

Prevalence and prognostic implications of hypertensive response to exercise in patients with hypertrophic cardiomyopathy.

Objective: Hypertensive response to exercise (HRE) is observed in patients with hypertrophic cardiomyopathy (HCM) with normal resting blood pressure (BP). However, the prevalence or prognostic implications of HRE in HCM remain unclear. Methods: In this study, normotensive HCM subjects were enrolled. HRE was defined as systolic BP > 210 mmHg in men or >190 mmHg in women, or diastolic BP > 90 mmHg, or an increase in diastolic BP > 10 mmHg during treadmill exercise. All participants were followed for subsequent development of hypertension, atrial fibrillation (AF), heart failure (HF), sustained ventricular tachycardia/fibrillation (VT/VF), and all-cause death. Six hundred and eighty HCM patients were screened. Results: 347 patients had baseline hypertension, and 333 patients were baseline normotensive. 132 (40%) of the 333 patients had HRE. HRE was associated with female sex, lower body mass index and milder left ventricular outflow tract obstruction. Exercise duration and metabolic equivalents were similar between patients with or without HRE, but the HRE group had higher peak heart rate (HR), better chronotropic response and more rapid HR recovery. Conversely, non-HRE patients were more likely to exhibit chronotropic incompetence and hypotensive response to exercise. After a mean follow-up of 3.4 years, patients with and without HRE had similar risks of progression to hypertension, AF, HF, sustained VT/VF or death. Conclusion: HRE is common in normotensive HCM patients during exercise. HRE did not carry higher risks of future hypertension or cardiovascular adverse outcomes. Conversely, the absence of HRE was associated with chronotropic incompetence and hypotensive response to exercise.

Gender-specific differences in susceptibility to low-dose methadone-associated QTc prolongation in patients with heroin dependence.

BACKGROUND: Methadone is associated with QTc prolongation and sudden death in susceptible patients. We sought to investigate whether there is a gender-based difference in susceptibility to methadone-associated QTc prolongation in heroin-dependent patients receiving a low-dose treatment regimen. METHODS: A cross-sectional assessment of dose and gender effects was performed in 283 patients (229 males, 54 females) who received a 12-lead ECG for QTc measurement 59 days (interquartile range: 36-288 days) after methadone treatment. To determine the effects of methadone over time, a subset of 150 participants (126 men, 24 women) who underwent a 12-lead ECG before and 37 days (interquartile range: 32-44 days) after methadone treatment were selected. RESULTS: In the cross-sectional study, a significant dose-dependent interaction between methadone and QTc (r = 0.201, P = 0.0007) was observed in individuals receiving a median methadone dose of 40 mg/day (interquartile range: 30-60 mg/day). The methadone-QTc correlation was significant in males (r = 0.210, P = 0.0014) but not in females (r = 0.164, P = 0.2363). The longitudinal assessment of methadone's effects over a 6-month period showed that 60.7% of individuals experienced an increase in QTc compared to baseline data. The adjusted QTc significantly increased from 418.5 to 426.9 milliseconds in males (P < 0.0001), compared to an insignificant change in females (437.7 milliseconds vs 441.1 milliseconds, P = 0.468). CONCLUSIONS: Low-dose methadone therapy shows dose-dependent QTc prolongation and is associated with significant QTc lengthening within 6 months of treatment initiation. Men are more susceptible than women to low-dose methadone-associated QTc prolongation.

Associations between Myocardial Diastolic Dysfunction and Cardiovascular Mortality in Chronic Kidney Disease: A Large Single-Center Cohort Study.

BACKGROUND: The clinical burden and prognostic role of diastolic dysfunction (DD), on the basis of the latest (2016) American Society of Echocardiography guidelines, remain unclear in patients with chronic kidney disease (CKD). Moreover, risk mapping of concomitant systolic dysfunction and DD to evaluate the hazard of cardiovascular (CV) mortality in patients with CKD remains unexplored. METHODS: This retrospective cohort study identified 20,257 adult patients who underwent comprehensive echocardiography between 2008 and 2016 at a tertiary medical center in central Taiwan. The patients were stratified by CKD stage, and 3-year CV mortality risk in each CKD stratum was estimated through multivariable Cox proportional-hazards modeling using left ventricular ejection fraction (LVEF) and DD grades on the basis of the 2016 American Society of Echocardiography guidelines as the main risk factors. RESULTS: Compared with patients with stages 1 and 2 CKD, those with stages 4 and 5 CKD had significantly lower left ventricular ejection fractions and more severe DD. Both left ventricular ejection fraction (<40% vs ≥60%; adjusted hazard ratio, 3.17; 95% CI, 2.54-3.97) and DD grade (severe DD vs normal diastolic function; adjusted hazard ratio, 3.33; 95% CI, 2.33-4.76) were independently associated with 3-year CV mortality in the entire study population and had comparable effect sizes. The corresponding adjusted hazard ratios further increased to 4.20 (95% CI, 2.45-7.21) and 4.54 (95% CI, 2.20-9.38) in patients with stages 4 and 5 CKD. Systolic dysfunction and DD demonstrated mutually augmentative effects on CV mortality. CONCLUSIONS: These findings suggest that the current practice of cardioprotection for patients with CKD should be prioritized at an early stage along with conventional nephroprotection.

Estimated left ventricular pressure-myocardial strain loop as an index of cardiac work predicts all-cause mortality in patients receiving regular hemodialysis.

BACKGROUND: A non-invasive method for left ventricular pressure-strain analysis has recently been introduced to provide information on cardiac work and detect subtler changes in cardiac function. This study aims to verify and construct a novel index that could accurately and independently predict the prognosis of patients with end-stage kidney disease (ESRD) receiving regular hemodialysis. METHODS: Patients with end-stage kidney disease (ESRD) receiving maintenance hemodialysis (4-h sessions, 3 times weekly for 3 months or more) and who underwent echocardiography between 2009 and 2014 in China Medical University Hospital, Taichung, Taiwan, were enrolled. Conventional (left ventricular ejection fraction, LVEF) and strain echocardiography parameters (global longitudinal strain, GLS; cardiac work index, CWI) in 102 eligible patients were analyzed and compared. CWI was calculated from estimated LV pressure-myocardial strain loop area. RESULTS: Results show that, while no significant differences were found between LVEF (0.57 ±â€¯0.12 vs. 0.59 ±â€¯0.09, P = 0.27) and GLS (-16.12 ±â€¯6.57% vs. -18.44 ±â€¯5.54%, P = 0.07), deceased patients had significantly lower CWI (1339 ±â€¯683.05 mmHg% vs. 1883.38 ±â€¯640.99 mmHg%, P = 0.0002) than surviving patients. The predictive values defined by area under the curve (AUC) of LVEF, GLS and CWI were 0.499, 0.619 and 0.724, respectively. CONCLUSION: In conclusion, CWI is an accurately independent predictor of all-cause mortality in ESRD patients receiving regular hemodialysis and may superior to the current predictors such as LVEF and GLS.

Validation and Comparison of the 2003 and 2016 Diastolic Functional Assessments for Cardiovascular Mortality in a Large Single-Center Cohort.

BACKGROUND: The prognostic performance of the diastolic dysfunction (DD) algorithms published by the Mayo Clinic research group in 2003 and the American Society of Echocardiography (ASE) and the European Association of Cardiovascular Imaging (EACVI) in 2016 in association with cardiovascular (CV) mortality was compared in this study. METHODS: A retrospective hospital cohort comprising 57,630 adults who had undergone comprehensive echocardiographic examinations between 2008 and 2016 was analyzed. All echocardiographic parameters were measured according to appropriate guidelines, and dates of CV death were verified using the national mortality database. The prognostic performance of the Mayo 2003 and ASE/EACVI 2016 algorithms in association with 3-year CV mortality was systematically investigated. RESULTS: The adjusted hazard ratio (aHR) for severe DD defined by Mayo 2003 (1.64; 95% CI, 1.02-2.64; P = .04) was less than that defined by ASE/EACVI 2016 (aHR, 2.46; 95% CI, 1.58-3.84; P < .001) compared with patients with normal diastolic function. According to the ASE/EACVI 2016 algorithm, the cumulative 3-year CV mortality rate was 2.4% (95% CI, 1.8%-3.0%) for normal diastolic function, 4.7% (95% CI, 4.0%-5.4%) for mild DD, 5.8% (95% CI, 5.0%-6.7%) for moderate DD, 8.3% (95% CI, 6.1%-10.5%) for severe DD, and 3.8% (95% CI, 2.8%-4.8%) for indeterminate DD, respectively (P < .001). The dose-mortality patterns following DD severity were observed only in the ASE/EAVCI 2016 classification. The risk for 3-year CV mortality in patients with concomitant left ventricular ejection fraction < 40% and severe DD was 7 times (aHR, 7.81 [95% CI, 3.81-16.0; P < .05] for Mayo 2003; aHR, 7.67 [95% CI, 4.61-12.8; P < .05] for ASE/EACVI 2016) higher than that in patients with left ventricular ejection fractions ≥ 60% and normal diastolic function. The absolute number of patients who were correctly reclassified by ASE/EAVCI 2016 was 23,181, corresponding to 42% of the absolute net reclassification index. CONCLUSIONS: DD and impaired left ventricular ejection fraction increased CV mortality risk in a mutually independent manner. The severity of DD on the basis of ASE/EACVI 2016 has a graded relationship with CV mortality in a large population cohort.

E/e' ratio and outcome prediction in hypertrophic cardiomyopathy: the influence of outflow tract obstruction.

Aims: Diastolic dysfunction is thought to be an important pathophysiologic component of hypertrophic cardiomyopathy (HCM). However, there are conflicting data on the potential value of the mitral E/e' ratio. We examined whether left ventricular outflow tract (LVOT) obstruction influences the value of E/e' in predicting outcomes in HCM. Methods and results: Patients who met diagnostic criteria for HCM were enrolled. Diastolic function was assessed with complete two-dimensional and Doppler echocardiography. A composite clinical outcome including new onset atrial fibrillation, sustained ventricular tachycardia/fibrillation, heart failure, transplantation, and death was examined over a mean follow-up period of 4.2 years. Among 604 patients, 206 patients had an E/e' level ≥20. Patients with higher septal E/e' level were older, with more severe NYHA class, and more severe LVOT obstruction. Higher E/e' was associated with worse event-free survival in non-obstructive group and total HCM cohort. In addition, E/e' and LVOT pressure gradient were highly correlated in non-obstructive and total HCM, but not in labile or obstructive group. During follow-up period, 95 patients underwent myectomy. Post-op E/e' correlated significantly with LVOT pressure gradient (R = 0.306, P = 0.004). In these patients, post-op E/e' was associated with worse event-free survival (log-rank P = 0.030). Conclusion: Assessment of E/e' is useful for risk stratification in HCM patients. Nevertheless, the predictive power is confounded by dynamic LVOT obstruction. Higher E/e' predicts worse clinical outcomes in non-obstructive HCM and in labile/obstructive after myectomy.

Myostatin does not regulate cardiac hypertrophy or fibrosis.

Myostatin is a negative regulator of muscle growth. Loss of myostatin has been shown to cause increase in skeletal muscle size and improve skeletal muscle function and fibrosis in the dystrophin-deficient mdx muscular dystrophy mouse model. We evaluated whether lack of myostatin has an impact on cardiac muscle growth and fibrosis in vivo. Using genetically modified mice we assessed whether myostatin absence induces similar beneficial effects on cardiac function and fibrosis. Cardiac mass and ejection fraction were measured in wild-type, myostatin-null, mdx and double mutant mdx/myostatin-null mice by high resolution echocardiography. Heart mass, myocyte area and extent of cardiac fibrosis were determined post mortem. Myostatin-null mice do not demonstrate ventricular hypertrophy when compared to wild-type mice as shown by echocardiography (ventricular mass 0.69+/-0.01 vs. 0.69+/-0.018 g) and morphometric analyses including heart/body weight ratio (5.39+/-0.45 vs. 5.62+/-0.58 mg/g) and cardiomyocyte area 113.67+/-1.5, 116.85+/-1.9 microm(2)). Moreover, absence of myostatin does not attenuate cardiac fibrosis in the dystrophin-deficient mdx mouse (12.2% vs. 12%). The physiological role of myostatin in cardiac muscle appears significantly different than that in skeletal muscle as it does not induce cardiac hypertrophy and does not modulate cardiac fibrosis in mdx mice.

Impact of peak provoked left ventricular outflow tract gradients on clinical outcomes in hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is traditionally classified based on a left ventricular outflow tract (LVOT) pressure gradient of 30mmHg at rest or with provocation. There are no data on whether 30mmHg is the most informative cut-off value and whether provoked gradients offer any information regarding outcomes. METHODS: Resting and provoked peak LVOT pressure gradients were measured by Doppler echocardiography in patients fulfilling guidelines criteria for HCM. A composite clinical outcome including new onset atrial fibrillation, ventricular tachycardia/fibrillation, heart failure, transplantation, and death was examined over a median follow-up period of 2.1years. RESULTS: Among 536 patients, 131 patients had resting LVOT gradients greater than 30mmHg. Subjects with higher resting gradients were older with more cardiovascular events. For provoked gradients, a bi-modal risk distribution was found. Patients with provoked gradients >90mmHg (HR 3.92, 95% CI 1.97-7.79) or <30mmHg (HR 2.15, 95% CI 1.08-4.29) have more events compared to those with gradients between 30 and 89mmHg in multivariable analysis. The introduction of two cut-off points for provoked gradients allowed HCM to be reclassified into four groups: patients with "benign" latent HCM (provoked gradient 30-89mmHg) had the best prognosis, whereas those with persistent obstructive HCM had the worst outcome. CONCLUSIONS: Provoked LVOT pressure gradients offer additional information regarding clinical outcomes in HCM. Applying cut-off points at 30 and 90mmHg to provoked LVOT pressure gradients further classifies HCM patients into low-, intermediate- and high-risk groups.

Usefulness of two-dimensional speckle strain for evaluation of left ventricular diastolic deformation in patients with coronary artery disease.

We investigated the influence of > or =70% luminal coronary artery stenosis on regional diastolic deformation at rest using 2-dimensional strain echocardiography. We prospectively imaged patients during/within 24 hours of coronary angiography. Longitudinal systolic (SRs), early (SRe), and late diastolic strain rates, systolic, early, and late diastolic strain and times to isovolumic relaxation and peak SRe were measured in the 3 major vascular territories. Regions subtended by > or =70% coronary stenosis were labeled ischemic. Ischemic regions were compared with the same region in patients without significant coronary stenosis. Of 61 enrolled patients (38 men), 39 had > or =70% coronary stenosis (1 vessel in 14, 2 vessels in 15, 3 vessels in 10), and 15 had normal coronary arteries. There were no significant differences between the normal and ischemic groups with regard to age (59 +/- 13 vs 64 +/- 10 years, p = 0.20), clinical variables (dyslipidemia, smoking, diabetes), systolic (130 +/- 26 vs 139 +/- 31 mm Hg, p = 0.38) or diastolic (72 +/- 13 vs 72 +/- 11 mm Hg, p = 0.81) blood pressure and ejection fraction (58 +/- 12% vs 56 +/- 11%, p = 0.66). SRs and SRe were significantly decreased in ischemic compared with normal regions in all vascular distributions. SRs and SRe together (values below cutoff) or SRe alone were the most specific (93%) and SRe or SRs below cutoff the most sensitive (93%) parameters for detecting ischemic regions. In conclusion, analysis of regional deformation by 2-dimensional strain echocardiography enables detection of significantly diseased coronary arteries at rest. Altered diastolic deformation at rest identifies regions subtended by > or =70% coronary stenosis with high specificity.

Comparison of usefulness of echocardiographic Doppler variables to left ventricular end-diastolic pressure in predicting future heart failure events.

We sought to determine whether the echocardiographic Doppler parameters of left ventricular diastolic dysfunction predict future heart failure (HF) events and, if so, which parameters best predict HF. We also examined whether the predictive ability of echocardiographic Doppler parameters was related to their prediction of left ventricular end-diastolic pressure (LVEDP). We studied patients who underwent cardiac catheterization and echocardiography performed within a 30-day period. The end point was HF, defined as new-onset or recurrent HF diagnosed by a physician and requiring the initiation or modification of treatment of HF. We identified 289 patients (mean age 63.5 +/- 12.6 years) with a mean follow-up of 10.9 +/- 10.2 months. A total of 24 HF events occurred. LVEDP was a significant predictor of HF univariately and independently in multiple regression models after adjustment for ejection fraction. In Cox models adjusted for age, gender, LVEDP, and ejection fraction, only the left atrial volume index and early mitral inflow to early diastolic tissue velocity (E/e') ratio remained predictive of HF. A multiple regression model, including all echocardiographic variables, showed a persistent, although attenuated, relation of early to late mitral inflow velocity (E/A) ratio and E/e' with LVEDP (p = 0.06 and p = 0.002, respectively). The addition of E/e' or the left atrial volume indexed to body surface area, but not E/A, to the clinical history and left ventricular ejection fraction provided incremental prognostic information. A LVEDP of > or =20 mm Hg, E/e' ratio of > or =15, and left atrial volume index of > or =23 ml/m(2) identified those with a higher risk of HF. In conclusion, invasively determined LVEDP is an independent predictor of future HF events. E/e' and the left atrial volume indexed to body surface area are the best independent predictors of future HF and provide prognostic information incremental to the clinical history and left ventricular ejection fraction.

Acute myocardial infarction with patent coronary artery after a long-distance flight--a case report.

Acute myocardial infarction is unusual in a young woman, especially with normal coronary arteriography. There are several mechanisms hypothesized, including coronary artery embolism, coronary spasm, illegal drug abuse and toxic condition. However, the etiology could be detected in only one third of these patients. Although air travel is known to precipitate deep vein thrombosis and pulmonary embolism, it is unclear whether it also causes myocardial infarction. We report a 37 year-old woman who had no risk factor for coronary artery disease, who suffered from acute myocardial infarction complicated with ventricular fibrillation after a long-distance flight across the Pacific Ocean from the United States to Taiwan. The coronary arteriogram disclosed patent coronary artery with slight intraluminal haziness in the proximal left anterior descending artery. The left ventriculogram demonstrated akinesia of anterolateral and apical segments with apical thrombus formation. We reviewed the related literature and considered the myocardial infarction in this patient was related to coronary thrombus formation after long-distance air travel.

Myopotential interference with a unipolar VDD pacemaker presenting with tachycardia and transient ventricular asystole.

Interference between myopotentials and pacemakers is well recognized, especially in a unipolar pacing system. This case report describes myopotential interference with an atrial synchronous ventricular inhibited (VDD) unipolar pacemaker in a 54-year-old woman. The interference caused both repetitive ventricular upper rate pacing and sometimes ventricular channel inhibition, resulting in palpitation and near syncope. Provocative tests elicited the myopotential interference reproducibly. The problem was partially corrected by further sensitivity adjustment.

Isolated congenital ventricular septal aneurysm in an adult--a case report.

Congenital ventricular septal aneurysm without ventricular septal defect is a very rare condition. We describe the clinical features of an adult case and the literature was reviewed. A 54-year-old woman experienced intermittent palpitation with rapid heart beating sensation for several years. The duration was only several seconds. There was neither congestive heart failure nor syncope history. Physical examination revealed mid-systolic click with grade II/VI systolic murmur at apical area. Echocardiography disclosed mitral valve prolapse with mild mitral regurgitation. A ventricular septal aneurysm bulging into right ventricle was found incidentally. Transesophageal echocardiographic and cardiac angiographic pictures of ventricular septal aneurysm were demonstrated. Since the patient was relatively asymptomatic, no surgical intervention was advised.