Poor Nutritional Status during Recovery from Acute Myocardial Infarction in Patients without an Early Nutritional Intervention Predicts a Poor Prognosis: A Single-Center Retrospective Study.

Whether malnutrition during the early phase of recovery from acute myocardial infarction (AMI) could be a predictor of mortality or morbidity has not been ascertained. We examined 289 AMI patients. All-cause mortality and composite endpoints (all-cause mortality, nonfatal stroke, nonfatal acute coronary syndrome, and hospitalization for acute decompensated heart failure) during the follow-up duration (median 39 months) were evaluated. There were 108 (37.8%) malnourished patients with GNRIs of less than 98 on arrival; however, malnourished patients significantly decreased to 91 (31.4%) during the convalescence period (p < 0.01). The incidence rates of mortality and primary composite endpoints were significantly higher in the malnourished group than in the well-nourished group both on arrival and during the convalescence period (All p < 0.05). Nutrition guidance significantly improved GNRI in a group of patients who were undernourished (94.7 vs. 91.0, p < 0.01). Malnourished patients on admission who received nutritional guidance showed similar all-cause mortality with well-nourished patients, whereas malnourished patients without receiving nutritional guidance demonstrated significantly worse compared to the others (p = 0.03). The assessment of GNRI during the convalescence period is a useful risk predictor for patients with AMI. Nutritional guidance may improve the prognoses of patients with poor nutritional status.

Objective Evaluation With Noncontrast Computed Tomography Can Reveal Calcified Plaque Solidity in Peripheral Artery Diseases.

PURPOSE: The presence of severely calcified plaque remains problematic in endovascular therapy, and no specific endovascular treatment strategy has been established. Estimating plaque solidity before the procedure may help operators penetrate calcified plaque with a guide wire. The aim of this study was to establish a method of measuring plaque solidity with noncontrast computed tomography (CT). METHODS: This retrospective, single-center study included consecutive patients who, between October 2020 and July 2022, underwent noncontrast 5 mm and 1 mm CTs before endovascular therapy to penetrate calcified plaque with a wire in the common femoral, superficial femoral, and popliteal arteries. Three cross-sectional CT slices were selected. To target a calcified plaque lesion, the operator identified a region of interest, which corresponded to 24×24 pixels, and Hounsfield unit (HU) values of each pixel were displayed on the CT image. The average HU values and the ratio of number of pixels of lower values (130-599 HU) represented plaque solidity. We used the Mann-Whitney-Wilcoxon rank-sum test and the chi-square test to compare the solidity of plaques penetrated and not penetrated by the wire. RESULTS: We evaluated 108 images of 36 calcified plaque lesions (in 19 patients). The wire penetrated 28 lesions (77.8%) successfully. The average HU value was significantly lower in the lesions that the wire penetrated than in the others, in both the 5 mm CT slices (434.7±86.8 HU vs 554.3±112.7 HU, p=0.0174) and 1 mm slices (497.8±103.1 HU vs 593.5±114.5 HU, p=0.0381). The receiver operating curve revealed that 529.9 and 533.9 HU in the 5 and 1 mm slices, respectively, were the highest values at which wires could penetrate. Moreover, at the lesions that were penetrates successfully, the ratio of number of lower HU value pixels was significantly higher both in 5 mm slice CTs (74.7±13.4 vs 61.7±13.1%, p=0.0347) and 1 mm (68.7±11.8 vs 57.1±11.4%, p=0.0174). CONCLUSION: The use of noncontrast CT to evaluate plaque solidity was associated with successful wire penetration of calcified lesions in peripheral arteries. CLINICAL IMPACT: This study revealed an association between the wire penetration inside calcified plaque and plaque solidity estimated using non-contrasted computed tomography. The mean Hounsfield unit values of three cross-sections in calcified plaques were associated with the successful wire penetration. This wire penetration difficulty is associated with extended procedure time, excessive radiation exposure, usage of extra contrast agents, and increased medical costs. Therefore, estimating calcified plaque solidity before procedure enables us to choose effective and lean procedures. In addition, to predict the success of dilating calcified plaque from the inside is also beneficial when the operator wants to avoid extra scaffold implantation for target lesions.

Impact of bystander cardiopulmonary resuscitation on neurological outcomes in patients undergoing veno-arterial extracorporeal membrane oxygenation.

BACKGROUND: Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) requires a large amount of economic and human resources. The presence of bystander cardiopulmonary resuscitation (CPR) was focused on selecting appropriate V-A ECMO candidates. RESULT: This study retrospectively enrolled 39 patients with V-A ECMO due to out-of-hospital cardiac arrest (CA) between January 2010 and March 2019. The introduction criteria of V-A ECMO included the following: (1) < 75 years old, (2) CA on arrival, (3) < 40 min from CA to hospital arrival, (4) shockable rhythm, and (5) good activity of daily living (ADL). The prescribed introduction criteria were not met by 14 patients, but they were introduced to V-A ECMO at the discretion of their attending physicians and were also included in the analysis. Neurological prognosis at discharge was defined using The Glasgow-Pittsburgh Cerebral Performance and Overall Performance Categories of Brain Function (CPC). Patients were divided into good or poor neurological prognosis (CPC ≤ 2 or ≥ 3) groups (8 vs. 31 patients). The good prognosis group had a significantly larger number of patients who received bystander CPR (p = 0.04). The mean CPC at discharge was compared based on the combination with the presence of bystander CPR and all five original criteria. Patients who received bystander CPR and met all original five criteria showed significantly better CPC than patients who did not receive bystander CPR and did not meet some of the original five criteria (p = 0.046). CONCLUSION: Considering the presence of bystander CPR help in selecting the appropriate candidate of V-A ECMO among out-of-hospital CA cases.

Trend in Age at the Initial Pacemaker Implantation in Patients With Bradyarrhythmia　- A 50-Year Analysis (1970-2019) in Japan.

BACKGROUND: This study investigated whether the age of patients undergoing pacemaker implantation is increasing.Methods and Results: This study retrospectively reviewed the consecutive cases of 3,582 patients who underwent an initial pacemaker implantation at our hospitals because of symptomatic bradyarrhythmias between 1970 and 2019. The exclusion criteria were: patients with AV block due to cardiac surgery or AV junction ablation, and patients aged <20 years. The patients were divided into 5×10-year groups: those treated in the 1970s (1970-1979), 1980s (1980-1989), 1990s (1990-1999), 2000s (2000-2009), and 2010s (2010-2019). A total of 3,395 patients satisfied the study criteria. The average age at which the patients underwent a first pacemaker implantation increased across the 10-year periods: 63.7±13.2 years in the 1970s, 66.2±12.6 years (1980s), 69.1±12.4 years (1990s), 72.0±11.1 years (2000s), and 75.8±10.0 years (2010s) and advanced significantly in the 1990s, 2000s, and 2010s compared to the 1970s (all P<0.001). The ratio of patients aged ≥80 and ≥90 years increased from 10.6% and 0% in the 1970 s to 38.2% (P<0.001) and 5.2% (P= 0.017) in the 2010s, respectively. CONCLUSIONS: The average age at initial pacemaker implantation increased by 12.1 years over the last 50 years in Japan. In particular, the ratios of ≥80 and ≥90 years as the patients age increased significantly.

A Case of ST-Elevation Acute Myocardial Infarction in a Nonhospitalized Patient with SARS-CoV-2 Pneumonia: Treatment with Primary Percutaneous Coronary Intervention.

We experienced a case of primary percutaneous coronary intervention for ST-elevation myocardial infarction (STEMI) with coronavirus disease 2019 (COVID-19) using appropriate infection prevention protocol. However, recanalization was difficult due to severe coagulopathy. Further researches are needed to clarify optimal treatment for STEMI in patients with COVID-19.

Heart Failure with Hyperthyroidism Demonstrating Discrepancy between the Clinical Course and B-type Natriuretic Peptide Levels.

A 35-year-old Japanese man was emergently admitted to our hospital with chief complaints of palpitation and dyspnea. He has been treated for Basedow's disease. He was diagnosed with acute decompensated heart failure, atrial fibrillation and thyrotoxicosis. We started anti-thyroid agents and a treatment for heart failure with beta blockers and diuretics under anti-coagulation therapy. His B-type natriuretic peptide levels remained high, although the heart failure had been compensated and the heart rate was well controlled while hyperthyroidism still existed. We should bear in mind that a discrepancy can exist between the clinical course and the B-type natriuretic peptide level in heart failure patients complicated with hyperthyroidism.

A proposal of clinical ECG index "vagal score" for determining the mechanism of paroxysmal atrioventricular block.

BACKGROUND: Paroxysmal atrioventricular block (P-AVB) is a well-known cause of syncope; however, its underlying mechanism is difficult to determine. This study aimed to evaluate a new ECG index, the "vagal score (VS)," to determine the mechanism of P-AVB. METHODS: We evaluated the VS in 20 patients with P-AVB (13 men, 7 women; aged 25-78 years [mean, 59.3 years]). The VS was developed by assigning 1 point each for the following: (1) no AVB or intraventricular conduction disturbance on the baseline ECG, (2) PR prolongation immediately before P-AVB, (3) sinus slowing immediately before P-AVB, (4) initiation of P-AVB by PP prolongation, (5) sinus slowing during ventricular asystole, and (6) resumption of AV conduction with PP shortening, and by assigning -1 point each for (7) the initiation of P-AVB by a premature beat, and (8) resumption of AV conduction by an escape beat. Based on the clinical situations and electrophysiologic findings, we considered the mechanism of P-AVB as vagally mediated or intrinsic conduction disease (ICD). RESULTS: The VS ranged from 5 to -2 points for each patient. Five patients with a definite vagally mediated P-AVB had high VSs (3-5 points). We observed characteristic ECG findings of ICD consisting of changes in AV conduction by an extrasystole and/or escape beat in only 5 of the 6 patients (83%) with a low VS (1 to -2). CONCLUSIONS: The VS is simple and potentially useful for determining the mechanism of P-AVB. P-AVB with a VS ≥3 strongly suggested a vagally mediated mechanism.

Effects of candesartan on electrical remodeling in the hearts of inherited dilated cardiomyopathy model mice.

Inherited dilated cardiomyopathy (DCM) is characterized by dilatation and dysfunction of the ventricles, and often results in sudden death or heart failure (HF). Although angiotensin receptor blockers (ARBs) have been used for the treatment of HF, little is known about the effects on postulated electrical remodeling that occurs in inherited DCM. The aim of this study was to examine the effects of candesartan, one of the ARBs, on cardiac function and electrical remodeling in the hearts of inherited DCM model mice (TNNT2 ΔK210). DCM mice were treated with candesartan in drinking water for 2 months from 1 month of age. Control, non-treated DCM mice showed an enlargement of the heart with prolongation of QRS and QT intervals, and died at t1/2 of 70 days. Candesartan dramatically extended the lifespan of DCM mice, suppressed cardiac dilatation, and improved the functional parameters of the myocardium. It also greatly suppressed prolongation of QRS and QT intervals and action potential duration (APD) in the left ventricular myocardium and occurrence of ventricular arrhythmia. Expression analysis revealed that down-regulation of Kv4.2 (Ito channel protein), KChIP2 (auxiliary subunit of Kv4.2), and Kv1.5 (IKur channel protein) in DCM was partially reversed by candesartan administration. Interestingly, non-treated DCM heart had both normal-sized myocytes with moderately decreased Ito and IKur and enlarged cells with greatly reduced K+ currents (Ito, IKur IK1 and Iss). Treatment with candesartan completely abrogated the emergence of the enlarged cells but did not reverse the Ito, and IKur in normal-sized cells in DCM hearts. Our results indicate that candesartan treatment suppresses structural remodeling to prevent severe electrical remodeling in inherited DCM.

Usefulness of running wheel for detection of congestive heart failure in dilated cardiomyopathy mouse model.

BACKGROUND: Inherited dilated cardiomyopathy (DCM) is a progressive disease that often results in death from congestive heart failure (CHF) or sudden cardiac death (SCD). Mouse models with human DCM mutation are useful to investigate the developmental mechanisms of CHF and SCD, but knowledge of the severity of CHF in live mice is necessary. We aimed to diagnose CHF in live DCM model mice by measuring voluntary exercise using a running wheel and to determine causes of death in these mice. METHODOLOGY/PRINCIPAL FINDINGS: A knock-in mouse with a mutation in cardiac troponin T (ΔK210) (DCM mouse), which results in frequent death with a t(1/2) of 70 to 90 days, was used as a DCM model. Until 2 months of age, average wheel-running activity was similar between wild-type and DCM mice (approximately 7 km/day). At approximately 3 months, some DCM mice demonstrated low running activity (LO: <1 km/day) while others maintained high running activity (HI: >5 km/day). In the LO group, the lung weight/body weight ratio was much higher than that in the other groups, and the lungs were infiltrated with hemosiderin-loaded alveolar macrophages. Furthermore, echocardiography showed more severe ventricular dilation and a lower ejection fraction, whereas Electrocardiography (ECG) revealed QRS widening. There were two patterns in the time courses of running activity before death in DCM mice: deaths with maintained activity and deaths with decreased activity. CONCLUSIONS/SIGNIFICANCE: Our results indicate that DCM mice with low running activity developed severe CHF and that running wheels are useful for detection of CHF in mouse models. We found that approximately half of ΔK210 DCM mice die suddenly before onset of CHF, whereas others develop CHF, deteriorate within 10 to 20 days, and die.

Multistep ion channel remodeling and lethal arrhythmia precede heart failure in a mouse model of inherited dilated cardiomyopathy.

BACKGROUND: Patients with inherited dilated cardiomyopathy (DCM) frequently die with severe heart failure (HF) or die suddenly with arrhythmias, although these symptoms are not always observed at birth. It remains unclear how and when HF and arrhythmogenic changes develop in these DCM mutation carriers. In order to address this issue, properties of the myocardium and underlying gene expressions were studied using a knock-in mouse model of human inherited DCM caused by a deletion mutation ΔK210 in cardiac troponinT. METHODOLOGY/PRINCIPAL FINDINGS: By 1 month, DCM mice had already enlarged hearts, but showed no symptoms of HF and a much lower mortality than at 2 months or later. At around 2 months, some would die suddenly with no clear symptoms of HF, whereas at 3 months, many of the survivors showed evident symptoms of HF. In isolated left ventricular myocardium (LV) from 2 month-mice, spontaneous activity frequently occurred and action potential duration (APD) was prolonged. Transient outward (I(to)) and ultrarapid delayed rectifier K(+) (I(Kur)) currents were significantly reduced in DCM myocytes. Correspondingly, down-regulation of Kv4.2, Kv1.5 and KChIP2 was evident in mRNA and protein levels. In LVs at 3-months, more frequent spontaneous activity, greater prolongation of APD and further down-regulation in above K(+) channels were observed. At 1 month, in contrast, infrequent spontaneous activity and down-regulation of Kv4.2, but not Kv1.5 or KChIP2, were observed. CONCLUSIONS/SIGNIFICANCE: Our results suggest that at least three steps of electrical remodeling occur in the hearts of DCM model mice, and that the combined down-regulation of Kv4.2, Kv1.5 and KChIP2 prior to the onset of HF may play an important role in the premature sudden death in this DCM model. DCM mice at 1 month or before, on the contrary, are associated with low risk of death in spite of inborn disorder and enlarged heart.