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To investigate the long-term efficacy of percutaneous transluminal pulmonary angioplasty (PTPA) in patients with Takayasu arteritis (TA) and pulmonary artery stenosis and pulmonary hypertension (PH). Data from 183 lesions from 79 surgeries performed on 32 patients with TA and PH were analyzed. Symptoms, laboratory investigation results, World Health Organization (WHO) functional class, 6-min walk distance (6 MWD), hemodynamic parameters, and prognosis were analyzed at baseline and follow-up. The mean (± SD) age of the 32 patients (28 female, 4 male) was 42.8 ± 11.9 years, and the median follow-up was 49.5 months (interquartile range, 26-71 months). Compared with baseline, changes in total bilirubin, N-terminal pro-brain natriuretic peptide (NT-proBNP) level, 6 MWD, and WHO score functional class demonstrated significant differences ( <0.001). Echocardiography findings, right and left ventricular diameter, tricuspid annular plane systolic excursion, and estimated pulmonary artery systolic pressure were all improved ( =0.016, <0.001, <0.001, =0.005, respectively). Importantly, repeat right heart catheterization revealed that mean pulmonary artery pressure, pulmonary vascular resistance, and cardiac index also improved significantly at follow-up ( <0.001, <0.001, and =0.011, respectively). Pulmonary angiography revealed post-procedure restenosis in 64 (35.0%) lesions underwent PTPA within three to six months. Among three patients who underwent stent implantation, one experienced restenosis. Two patients died during the follow-up period, one from aggravation of right heart failure after lung infection, and the other in a traffic accident. Results of this study indicated that PTPA significantly improved clinical symptoms, exercise tolerance, and hemodynamic parameters in patients with TA pulmonary artery stenosis and PH. More importantly, reperfusion pulmonary edema significantly decreased, and no patient died of PTPA-related complications with guidance from the pressure wire.

Current guideline for evaluating diastolic function requires multiple parameters to identify patients with elevated left ventricular end-diastolic pressure (LVEDP). However, the intermediate result still exists and may cause LVEDP undetermined. Previous studies have shown intraventricular pressure difference (IVPDs) are required for normal LV filling, but the relationship between IVPDs and LVEDP is unknown. In this study, we analyzed the relationship between IVPDs and LVEDP in 54 patients with coronary artery disease (CAD). LVEDP was prospectively measured at the time of coronary intervention and LVEDP > 15 mmHg was considered as elevated LV filling pressure. Simultaneous echocardiographic data was collected prior to the intervention. The relative intraventricular pressure was calculated using the vector flow mapping method. The IVPD was defined as the pressure difference from the apex to the base of LV. From 54 patients presenting with CAD, elevated LVEDP occurred in 30(55.6%). To analyze the changing trend of IVPD with LVEDP, CAD patients were further divided into group I with normal LVEDP (12.7 ± 3.1 mmHg) and group II with elevated LVEDP (26.0 ± 7.2 mmHg). In early diastole, both isovolumic relaxation period and rapid filling period showed decreased IVPD in CAD patients, but only the reduction in isovolumic relaxation period (IVPD-IVR) was statistical different between patients with elevated LVEDP and normal LVEDP (1.03 ± 0.42 mmHg vs. 2.25 ± 1.21 mmHg, p  < 0.01). IVPD-IVR had the best correlation with LVEDP ( r =-0.499, p  < 0.01) among IVPDs. Lower IVPD-IVR was associated with higher risk of elevated LVEDP. Evaluating IVPD-IVR might improve the diagnostic algorithm for predicting elevated LVEDP.

Obstructive sleep apnea (OSA) is much common and associated with worse clinical outcomes in patients with hypertrophic cardiomyopathy (HCM), however, the diagnosis of OSA in HCM is still insufficient. We aim to investigate the clinical predictors of OSA in a large series of patients with HCM. A total of 589 patients with HCM who underwent sleep evaluations were retrospectively enrolled. Data from clinical characteristics and polysomnography studies were recorded. OSA was present in 346 patients (58.7%). Patients who had OSA were older, more likely to be male and had more clinical comorbidities such as hypertension, atrial fibrillation and cardiac remodeling. Multivariate logistic analyses showed that male, age, body mass index, hypertension and left ventricular outflow tract obstruction were significant factors associated with OSA. The area under the ROC curve (AUC) was 0.78 (95% CI 0.74–0.82; P < 0.001). These factors were also able to identify moderate to severe OSA with an AUC of 0.77 (95% CI 0.73–0.81; P < 0.001). These findings suggest that identifying HCM patients with high risk for OSA is feasible using characteristics from clinical practices and clinicians should have no hesitate to conduct sleep test in these patients.

Atrial fibrillation (AF) is the most common arrhythmia and potentially increase the risk of embolic stroke and aggravate progressive heart failure in patients with hypertrophic cardiomyopathy (HCM). Recent studies demonstrated that epicardial adipose tissue (EAT) was closely associated with AF in general population. However, the relationship between EAT and AF in HCM patients remains unclear. A total of 93 consecutive patients with hypertrophic obstructive cardiomyopathy (HOCM) at Fuwai Hospital were enrolled in our study. There were 18 patients with AF and 75 patients without it. Cardiac magnetic resonance (CMR) imaging was performed in all participants. EAT volume (EATV) and left atrial volume (LAV) were determined by E-3D medical model software. HOCM patients with AF had significantly greater EATV index (EATVI, P < 0.001), LAV index (LAVI, P < 0.001) and left ventricular end-systole volume index (LVESVI, P = 0.039), and lower left ventricular ejection fraction (LVEF, P = 0.002). In multivariable logistic regression analysis, EATVI, LAVI, and LVEF remained independent determinants of AF occurrence (OR = 1.023, 95% CI, 1.003–1.043, P = 0.023, OR = 1.043, 95% CI, 1.012–1.075, P = 0.006, and OR = 0.887, 95% CI, 0.818–0.962, P = 0.004, respectively). Furthermore, receiver operating characteristic (ROC) curve analysis demonstrated that integration of EATVI, LAVI and LVEF provided better discriminatory performance for incident AF in HOCM patients with a high sensitivity of 94.4% and a specificity of 69.3% (AUC = 0.864, 95% CI, 0.771–0.958, P < 0.001). EATVI is an independent predictor of the presence of AF, and integration of EATVI, LVEF and LAVI determined by CMR provide greater discriminatory performance for identifying AF in HOCM patients.

There are controversies on optimal stenting strategy regarding true left main (LM) bifurcation lesions. The present study compared 1- and 2-stenting strategy for patients with true LM bifurcation lesions as differentiated by DEFINITION criteria. 928 patients with true LM bifurcation lesions (Medina 1,1,1 or 0,1,1) treated with DES were enrolled consecutively. 297 (32.0%) patients were identified as complex LM bifurcation, and 631 (68.0%) patients into simple LM bifurcation group according to DEFINTION criteria. Patients in complex vs. simple LM bifurcation group had significantly higher major adverse cardiac event (MACE, including cardiac death, myocardial infarction [MI] and ischemia-driven target vessel revascularization) rate at 30 days (7.8% vs. 4.0%, p = 0.01), 1 year (10.3% vs. 6.4%, p = 0.04), and numerically at 3 years (14.2% vs. 10.1%, p = 0.07), which was mainly driven by increased MI. Moreover, patients in the 2-stent strategy group had strong trend towards lower incidence of cardiac death in both complex LM bifurcation group (2.0% vs. 5.9%, p = 0.08) and simple LM bifurcation group (1.9% vs. 4.5%, p = 0.07). In conclusion, the complex bifurcation lesion criteria established in DEFINITION study was able to risk-stratify LM bifurcation patients. Two-stent technique yielded numerically lower 3-year cardiac mortality regardless of LM bifurcation complexity.

Background To investigate the relationship between fragmented QRS (fQRS) quantified by a new method and myocardial fibrosis (MF) and the diagnostic value of quantitative fQRS (Q-fQRS) to detect MF in hypertrophic obstructive cardiomyopathy (HOCM) patients based on histological validation. Methods We performed a retrospective study that included 69 patients with HOCM who underwent ventricular septal surgery. Nine individuals who died from accidents were studied as a control reference for the histological parameters. Septal myocardium samples were subjected to Masson’s trichrome staining to quantify the collagen volume fraction (CVF). An fQRS pattern was defined as the presence of additional R waves or RSR’, evidenced by notched R or S wave on electrocardiography (ECG). The Q-fQRS was quantified as the total amount of deflections in the QRS complex in all 12 routine ECG leads together. Cardiac magnetic resonance imaging was conducted, and late gadolinium enhancement (LGE) was measured at 2, 4, 6 and 8 standard deviations (SDs). Results Of the 69 patients, fQRS was documented in 38 (55.1%) patients, the mean number of leads with fQRS was 3.7 ± 1.6, and the mean Q-fQRS was 17 ± 7.2. Compared with HOCM patients without fQRS, HOCM patients with fQRS had a higher CVF and more LGE at 6 SD ( P  < 0.001; P  = 0.040). Q-fQRS was correlated with CVF (r = 0.640, P  < 0.001), and Q-fQRS showed the best correlation with LGE measured at 8 SD (r = 0.379, P  = 0.002). Multivariate regression analyses revealed that Q-fQRS was independently associated with the extent of CVF in HOCM patients after adjusting for age, sex, body surface area and the extent of LGE at 6 SD ( P  < 0.001). When the patients were divided into subgroups with normal CVF or high CVF according to the CVF in controls, Q-fQRS and LGE at 6SD showed similar diagnostic value in detecting patients with high CVF, with sensitivities of 66.7% vs 68.6%, specificities of 76.7% vs 72.4%, and accuracies of 71% vs 70.3%. Conclusions HOCM patients with fQRS showed more extensive MF. Q-fQRS was an independent predictor for MF and had a good diagnostic value, with a sensitivity of 66.7% and specificity of 76.7%, in identifying patients with higher fibrotic burden.

Post-discharge management of coronary artery disease (CAD) remains clinically challenging, with digital healthcare’s efficacy underexplored. This study analyzed 16,797 CAD patients enrolled in the HeartMed Digital Management System (June 2018–September 2022), comparing outcomes between a digital management (DM, n = 4,713) and conventional management (CM, n = 12,084) cohort over 12 months. Cox models adjusted for confounders revealed significantly reduced all-cause mortality in the DM group (1.6% vs. 2.7%; HR 0.58, 95% CI 0.45–0.75, p < 0.001) and lower risks for major adverse cardiovascular events (MACCE: 6.4% vs. 9.2%; HR 0.67, 0.59–0.77, p < 0.001), cardiovascular death (HR 0.70, 0.51–0.95), myocardial infarction (HR 0.38, 0.29–0.50), recurrent angina (HR 0.75, 0.65–0.87), revascularization (HR 0.84, 0.71–0.99), and readmissions (HR 0.76, 0.68–0.84) (p < 0.05 for all). Digital healthcare demonstrates superior post-discharge optimization of CAD outcomes, significantly attenuating mortality and morbidity.

Both high-sensitivity cardiac troponin T and B-type natriuretic peptide are useful in detecting myocardial fibrosis, as determined by late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR), in patients with non-obstructive hypertrophic cardiomyopathy. However, their values to predict myocardial fibrosis in hypertrophic obstructive cardiomyopathy (HOCM) remain unclear. We investigated the role of N-Terminal Pro-B-Type Natriuretic Peptide (NT-proBNP) and cardiac troponin I (cTnI) to identify LGE-CMR in patients with HOCM. Peripheral concentrations of NT-proBNP and cTnI were determined in patients with HOCM (n = 163; age = 47.2 ± 10.8 years; 38.7% females). Contrast-enhanced CMR was performed to identify and quantify myocardial fibrosis. LGE was detected in 120 of 163 patients (73.6%). Patients with LGE had significantly higher levels of NT-proBNP and cTnI than those without LGE (1386.2 [904.6-2340.8] vs. 866.6 [707.2-1875.2] pmol/L, P = 0.003; 0.024 [0.010-0.049] vs. 0.010 [0.005-0.021] ng/ml, P <0.001, respectively). The extent of LGE was positively correlated with log cTnI (r = 0.371, P <0.001) and log NT-proBNP (r = 0.211, P = 0.007). On multivariable analysis, both log cTnI and maximum wall thickness (MWT) were independent predictors of the presence of LGE (OR = 3.193, P = 0.033; OR = 1.410, P < 0.001, respectively), whereas log NT-proBNP was not. According to the ROC curve analysis, combined measurements of MWT ≥21 mm and/or cTnI ≥0.025 ng/ml indicated good diagnostic performance for the presence of LGE, with specificity of 95% or sensitivity of 88%. Serum cTnI is an independent predictor useful for identifying myocardial fibrosis, while plasma NT-proBNP is only associated with myocardial fibrosis on univariate analysis. Combined measurements of serum cTnI with MWT further improve its value in detecting myocardial fibrosis in patients with HOCM.

Background: Rapid progression of coronary non-target lesions is essential for the determination of future cardiovascular events. Clinical factors that predict rapid progression of non-target lesions are unclear. The purpose of this study was to identify the clinical predictors of rapid progression and revascularization of coronary non-target lesions. Methods: Consecutive patients with coronary heart disease who had undergone two serial coronary angiograms were enrolled. All coronary non-target lesions were identified and evaluated at both procedures. Multivariable Cox regression analysis was used to investigate the clinical risk factors associated with rapid progression or revascularization of coronary non-target lesions. Results: A total of 1255 patients and 1670 lesions were enrolled. In this cohort of patients, 239 (19%) had rapid progression and 186 (14.8%) underwent revascularization. At the lesion level, 251 (15.0%) had rapid progression and 194 (11.6%) underwent revascularization. The incidence of lesion revascularization and myocardial infarction was significantly higher in patients with rapid progression. In multivariable analyses, hypertension (hazard ratio [HR], 0.76; 95% confidence interval [95% CI], 0.58–1.00; p = 0.049), ST-segment elevation myocardial infarction (STEMI) (HR, 1.46; 95% CI, 1.03–2.07; p = 0.035), glycosylated hemoglobin (HR, 1.16; 95% CI, 1.01–1.33; p = 0.039) and lesion classification (B2/C versus A/B1) (HR, 1.73; 95% CI, 1.27–2.35; p = 0.001) were significant factors associated with rapid progression. The level of triglycerides (HR, 1.10; 95% CI, 1.00–1.20; p = 0.040) and lesion classification (B2/C versus A/B1) (HR, 1.53; 95% CI, 1.09–2.14; p = 0.014) were predictors of lesion revascularization. Conclusions: Hypertension, STEMI, glycosylated hemoglobin and lesion classification may be used as predictors of rapid progression of coronary non-target lesions. The level of triglyceride and lesion classification may predict the revascularization of non-target lesions. In order to prevent future cardiovascular events, increased attention should be paid to patients with these factors.