Chronic phase improvements in electrocardiographic and echocardiographic manifestations of left ventricular hypertrophy after alcohol septal ablation for drug-refractory hypertrophic obstructive cardiomyopathy.

After alcohol septal ablation (ASA), regression of left ventricular hypertrophy (LVH) has been observed in several studies using echocardiography or cardiac magnetic resonance, and favorable changes of myocardial excitation have been expected. However, no studies have focused on the alteration of electrocardiography (ECG) findings after ASA. Therefore, we evaluated serial changes in ECG parameters during the chronic phase after ASA for drug-refractory hypertrophic obstructive cardiomyopathy (HOCM). From 1998 to 2014, we performed 187 ASA procedures in 157 drug-refractory HOCM patients. After excluding patients who underwent dual-chamber pacing therapy and who underwent staged or repeat ASA within 2 years after the index ASA, 25 patients without bundle branch block and additional pacemaker implantation were enrolled in the main study group. ECGs, echocardiograms, and clinical follow-up data were evaluated at baseline and, 1, 6, 12, and 24 months after ASA. Patients with bundle branch block or additional pacemaker implantation were assigned in a referential group (n = 79), in which the echocardiographic changes between baseline and at 1 year were evaluated. Sokolow-Lyon index (SLi), Cornell index, and total 12-lead QRS amplitude significantly decreased during 2-year follow-up after ASA. SLi and Cornell index significantly decreased from 6 to 12 months (p < 0.05 vs. p < 0.01). Changes in SLi were significantly associated with changes in the interventricular septal thickness (r = 0.54, p < 0.005), left ventricular mass index (r = 0.40, p = 0.050), and peak creatine phosphokinase level (r = -0.41, p = 0.042), but not in the Cornell index and 12-lead QRS amplitude. In the comparison between baseline and at 1 year, significant improvements in the interventricular septal thickness, posterior wall thickness, left atrial size, E/A ratio, and E/e' were observed in the echocardiographic study. Changes of SLi reflected regression of LVH after ASA with the best correlation. During the chronic phase after ASA, LVH regression was confirmed by echocardiographic and ECG parameters.

Are atherosclerotic risk factors associated with a poor prognosis in patients with hyperuricemic acute heart failure? The evaluation of the causal dependence of acute heart failure and hyperuricemia.

Atherosclerosis induces the elevation of uric acid (UA), and an elevated UA level is well known to lead to a poor prognosis in patients with acute heart failure (AHF). However, the prognostic value of atherosclerotic risk factors in hyperuricemic AHF patients remains to be elucidated. The data from 928 patients who were admitted to the intensive care unit (ICU) at Nippon Medical School Chiba Hokusoh Hospital between January 2001 and December 2014, and whose serum UA levels were measured were screened. A total of 394 AHF patients with hyperuricemia were enrolled in this study. The patients were assigned to a low-risk group (≤1 atherosclerosis risk factor) and a high-risk group (≥2 atherosclerosis risk factors) according to their number of risk factors. The patients in the low-risk group were more likely to have dilated cardiomyopathy, clinical scenario 3 than those in the high-risk group. The serum total bilirubin, blood urea nitrogen, C-reactive protein, and brain-type natriuretic peptide levels were significantly higher in the low-risk group than the high-risk group (p < 0.001, p = 0.005, p = 0.003, and p = 0.008, respectively). A multivariate Cox regression model revealed that the number of risk factors (number = 1, HR (hazard ratio) 0.243, 95 % CI 0.096-0.618, p = 0.003; number = 2, HR 0.253, 95 % CI 0.108-0.593, p = 0.002; number ≥3, HR 0.209, 95 % CI 0.093-0.472, p < 0.001), eGFR (per 1.0 mmol/l increase) (HR 0.977, 95 % CI 0.961-0.994, p = 0.007), and serum UA level (per 1 mg/dl increase) (HR 1.270, 95 % CI 1.123-1.435, p < 0.001) was an independent predictor of 1-year mortality. The prognosis, including all-cause death and HF events, was significantly poorer among the low-risk patients than among the high-risk patients. Atherosclerotic risk factors were not associated with a poor prognosis in patients with hyperuricemic AHF.

Matrix Metalloproteinase-9 as a Marker for Plaque Rupture and a Predictor of Adverse Clinical Outcome in Patients with Acute Coronary Syndrome: An Optical Coherence Tomography Study.

OBJECTIVES: The present study sought to clarify the relationship between matrix metalloproteinase-9 (MMP-9) levels and plaque morphology demonstrated by optical coherence tomography (OCT), and to examine their prognostic impacts in patients with acute coronary syndrome (ACS). METHODS: MMP-9 levels were measured for patients with ACS (n = 249). Among 249 patients, 120 with evaluable OCT images were categorized into patients with ruptured plaques (n = 65) and those with nonruptured plaques (n = 55) on the basis of culprit lesion plaque morphology demonstrated by OCT. RESULTS: MMP-9 levels on admission were significantly higher in the rupture group than in the nonrupture group (p = 0.029). Although creatine kinase-MB (CK-MB) on admission was comparable between the groups, peak CK-MB was higher in the rupture group than in the nonrupture group (p < 0.001). By receiver operating characteristic curve analysis, the optimal cut-off value of MMP-9 to detect ruptured plaques was 65.5 ng/ml (p = 0.029). There was a nonstatistically significant trend toward increased cardiac death at 2 years (5.9 vs. 1.0%, p = 0.059) in patients with high MMP-9 (≥65.5 ng/ml) compared to those with low MMP-9 (<65.5 ng/ml). CONCLUSIONS: MMP-9 can differentiate ACS with ruptured plaques from nonruptured plaques, and MMP-9 may be a valuable predictor of long-term cardiac mortality in patients with ACS reflecting plaque rupture.

Prognostic impact of plasma volume status during hospital admission in patients with acute decompensated heart failure.

AIMS: Plasma volume status (PVS), a measure of plasma volume, has been evaluated as a prognostic marker for chronic heart failure. Although the prognostic value of PVS has been reported, its significance in patients with acute decompensated heart failure (ADHF) admitted to the cardiovascular intensive care unit (CICU) remains unclear. In this study, we examined the relationship between PVS and long-term mortality in patients with ADHF admitted to the CICU. METHODS: Between January 2018 and December 2020, 363 consecutive patients with ADHF were admitted to the Nippon Medical School Hospital CICU. Of the 363 patients, 206 (mean age, 74.9 ± 12.9 years; men, 64.6%) were enrolled in this study. Patients who received red blood cell transfusions, underwent dialysis, were discharged from the CICU or died in the hospital were excluded from the study. We measured the PVS of the patients at admission, transfer to the general ward (GW) and discharge using the Kaplan-Hakim formula. The patients were assigned to four groups according to the quartiles of their PVS measured at each of the three abovementioned timepoints. We examined the association between PVS and all-cause mortality during the observation period (1134 days). The primary endpoint of this study was all-cause mortality. RESULTS: The Kaplan-Meier analysis showed that the high PVS group had a significantly higher mortality rate at admission, transfer to the GW and discharge than the other groups (log-rank test: P = 0.016, P = 0.005 and P < 0.001, respectively). Univariate Cox regression analysis showed that age, body mass index, history of heart failure, use of beta-blockers, albumin level, blood urea nitrogen level, N-terminal pro-brain natriuretic peptide level and left ventricular ejection fraction were significantly different among the PVS groups and thus were not significant prognostic factors for ADHF. Furthermore, the multivariate analysis revealed that PVS at discharge [hazard ratio (HR) = 1.06 (1.00-1.12), P = 0.048] was an independent poor prognostic factor for ADHF. CONCLUSIONS: This study highlights the effect of PVS measured at different timepoints on the prognoses of ADHF patients. Regular assessment of PVS, particularly at discharge, is crucial for optimising patient management and achieving favourable outcomes in cases of ADHF.

A case of acute myocardial infarction due to coronary artery compression by mediastinal hematoma associated with thoracic aortic aneurysm rupture.

A 76-year-old woman was admitted to our department for pneumonia. Although she gradually recovered, she complained of chest and back pain and went into shock. Electrocardiogram showed ST-segment elevation in the inferior leads; thus, an acute inferior myocardial infarction (MI) was strongly suspected. Emergent coronary angiography revealed subtotal right coronary artery (RCA) occlusion, and intravascular ultrasound showed flattening of the RCA ostium. Although the coronary artery flow improved after percutaneous coronary intervention with rescue stent implantation, the patient was still in a prolonged state of shock. Contrast-enhanced computed tomography revealed a ruptured thoracic aortic aneurysm (TAA) with a massive posterior mediastinal hematoma. We presumed that the acute MI and shock were caused by compression of the RCA ostium by the mediastinal hematoma and hemorrhage with TAA rupture, respectively. The patient was urgently transferred to another hospital for surgery. To the best of our knowledge, there has been no report on acute MI due to coronary artery compression by a mediastinal hematoma associated with TAA rupture. A staged therapeutic approach, involving preoperative coronary stent implantation, could be used to save the patient. .

Comparison of Coronary Culprit Lesion Morphology Determined by Optical Coherence Tomography and Relation to Outcomes in Patients Diagnosed with Acute Coronary Syndrome During Winter -vs- Other Seasons.

Patients diagnosed with acute coronary syndrome (ACS) during winter have worse outcomes; however, mechanisms driving this trend are unclear. We examined coronary culprit lesion morphologies using optical coherence tomography (OCT). Features and outcomes were retrospectively compared between patients admitted with ACS in winter (W-ACS; n = 390) and in other seasons (O-ACS; n = 1,027). Angiography and OCT results were analyzed in patients who underwent OCT examination (173 patients in W-ACS and 450 in O-ACS). On initial angiography, minimum lumen diameter was smaller (median; 0.12 mm vs 0.25 mm, p = 0.021) and Thrombolysis in myocardial infarction flow grade was worse (Thrombolysis in myocardial infarction 0/1; 57% vs 44%, p = 0.005) in W-ACS. OCT performed before coronary interventions or just after intracoronary thrombectomy showed that plaque rupture (56% vs 46%) and calcified nodules (8% vs 5%) were more prevalent, and plaque erosion (37% vs 49%) was less prevalent in W-ACS (p = 0.039 for all 3 variables). At 2-year follow-up for all admitted ACS patients, Kaplan-Meier estimates showed higher cardiac mortality in W-ACS (11.8% vs 8.3%, p = 0.043). Multivariate Cox proportional hazard analysis showed that patients in W-ACS group had a 1.5-fold increased risk of cardiac death within 2 years after adjusting for traditional cardiovascular risk factors (hazard ratio, 1.54 [95% confidence interval, 1.06 to 2.23]; p = 0.024). In conclusion, patients diagnosed with ACS during winter had worse angiographic results and OCT revealed less plaque erosion (more plaque rupture or calcified nodules) at the culprit lesions, which may be partly associated with worse cardiac mortality within 2 years.

Usefulness of Non-Anteroseptal Region Left Ventricular Hypertrophy Using Cardiac Magnetic Resonance to Predict Repeat Alcohol Septal Ablation for Refractory Obstructive Hypertrophic Cardiomyopathy.

We evaluated a cohort of patients treated with alcohol septal ablation (ASA) to identify predictive factors for repeat ASA. We compared 15 patients who underwent repeat ASA procedures (group R) with 69 patients not requiring repeat procedures (group S) in terms of clinical parameters and morphologic cardiac magnetic resonance. Group R showed higher number of hypertrophic segments (thickness ≥15 mm) in the basal left ventricular level (2.8 ± 1.7 vs 1.7 ± 0.8, p = 0.009) than group S. In the multivariate analysis, diuretics use (adjusted odds ratio 5.8, 95% confidential interval [CI] 1.04 to 32.2, p = 0.045) and the number of non-anteroseptal extended hypertrophy segments at the basal level were independent predictors of a repeat ASA procedure (adjusted odds ratio 3.64/segment, 95% CI 1.40 to 9.4, p = 0.008). One repeat ASA among 21 patients without non-anteroseptal hypertrophy and 1 repeat ASA among 29 patients without posteroseptal hypertrophy were observed; however, 7 of the 14 patients with ≥2 segments of non-anteroseptal hypertrophy received repeat ASA. In conclusion, cardiac magnetic resonance-based cross-sectional investigation elucidated non-anteroseptal hypertrophy (≥2 segments) to be a crucial predictor of repeat ASA. ASA is useful for patients with regional hypertrophy in the basal anteroseptal, but not posteroseptal region, and without heart failure requiring diuretics.

The prognostic impact of uric acid in patients with severely decompensated acute heart failure.

BACKGROUND: The serum level of uric acid (UA) is a well-known prognostic factor for heart failure (HF) patients. However, the prognostic impact of hyperuricemia and the factors that induce hyperuricemia in acute HF (AHF) patients are not well understood. METHODS AND RESULTS: Eight hundred eighty-nine AHF patients were enrolled in this study. The patients were assigned into a low UA group (UA≤7.0mg/dl, n=495) or a high UA group (UA>7.0mg/dl, n=394) according to their UA level on admission. A Kaplan-Meier curve showed that the survival rate of the low UA group was significantly higher than that of the high UA group. A multivariate Cox regression model identified that a high UA level (HR: 1.192, 95%CI 1.112-1.277) was an independent predictor of 180-day mortality. A multivariate logistic regression model for a high serum UA level on admission indicated that chronic kidney disease (CKD) (OR: 2.030, 95%CI: 1.298-3.176, p=0.002) and the administration of loop diuretics before admission (OR: 1.556, 95%CI: 1.010-2.397, p=0.045) were independent factors. The prognosis, including all-cause death and HF events, was significantly poorer among patients who had a high UA level who had previously used loop diuretics and among CKD patients with a high UA level than among other patients. CONCLUSIONS: The serum UA level was an independent predictor in patients who were hospitalized during an emergent situation for AHF. An elevated serum UA level on admission was associated with the presence of CKD and the use of loop diuretics. These factors were also associated with adverse outcomes in hyperuricemic patients with AHF.