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Rehabilitation based on guided walking is effective to recover activity of daily living (ADL) in frail older adults, even octogenarians. However, muscle dysfunction obviously reflects disability, and few studies have focused on ADL recovery by rehabilitation. We employed the state of muscle dysfunctions proposed by the Asian Working Group for Sarcopenia (AWGS) in 2019 and attempted to clarify the relation between the overlapping dysfunctions and the feasibility of ADL recovery after rehabilitation. In total, 297 frail older patients (the mean age: 82.8 years, 46.1% of patients were male) participated in a walking-guided rehabilitation program to achieve the goal of ambulatory discharge. Muscle dysfunction was categorized by four standardized methods at the start of rehabilitation (grip strength, gait speed, time of five sit-to-stand, and short physical performance battery: SPPB), according to the AWGS proposal. ADLs were monitored by Barthel index before admission, at the start of rehabilitation, and at discharge. At least one dysfunction was present in 95.3% of patients. If a single patient had three or more muscle dysfunction, the ADLs recovery was significantly limited (interaction: p < 0.05). The overlapped counts of AWGS muscle dysfunction helps to predict inverse feasibility of ADL recovery in frail older patients through rehabilitation. [ABSTRACT FROM AUTHOR]

Tissue macrophages can be activated by endogenous danger signals released from cells that are stressed or injured, leading to infiltration of inflammatory macrophages and neutrophils. We postulated that macrophage-related markers might be closely associated with the existence of endogenous danger signals, reflecting ongoing tissue injury in the absence of foreign substances. This study was designed to assess the ability of macrophage-related markers in endomyocardial biopsies to predict ongoing cardiac injury in non-inflammatory myocardial diseases. We examined levels of macrophage-related markers (CD68, CD163, CD45) in endomyocardial biopsies from patients ( n = 86) with various myocardial diseases by quantitative reverse transcription-polymerase chain reaction ( n = 78) and immunohistochemistry ( n = 56). Thirty-three patients without inflammatory cardiac disease such as myocarditis and sarcoidosis were classified as 'improved' or 'non-improved' defined as a 10 % increase in left ventricular ejection fraction by echocardiograph and a value greater than 30 % at the time of follow-up. All macrophage-related (MacR) markers levels were not higher in non-improved dilated cardiomyopathy (DCM) patients than improved patients. However, patients with cardiac amyloidosis, cardiac Fabry disease, mitochondrial cardiomyopathy, and biventricular arrhythmogenic right ventricular cardiomyopathy (ARVC), which were categorized as 'non-improvement diseases,' had elevated macrophage-related markers compared to improved patients. Macrophage-related markers levels were increased in endomyocardial biopsy samples of patients with intractable myocardial diseases such as amyloidosis, mitochondrial disease, Fabry disease, and biventricular ARVC. [ABSTRACT FROM AUTHOR]

Mechanical alternans (MA) is frequently observed in patients with heart failure, and is a predictor of cardiac events. However, there have been controversies regarding the conditions and mechanisms of MA. To clarify heart rate-dependent contractile properties related to MA, we performed incremental right atrial pacing in 17 idiopathic dilated cardiomyopathy (DCM) patients and in six control patients. The maximal increase in left ventricular d P/d t during pacing-induced tachycardia was assessed as the force gain in the force-frequency relationship (FG-FFR), and the maximal increase in left ventricular d P/d t of the first post-pacing beats was examined as the force gain in poststimulation potentiation (FG-PSP). As a result, MA was induced in 9 DCM patients (DCM MA(+)) but not in the other 8 DCM patients (DCM MA(−)), and not in any of the control patients. DCM MA(+) had significantly lower FG-FFR (34.7 ± 40.9 vs 159.4 ± 103.9 mmHg/s, P = 0.0091) and higher FG-PSP (500.0 ± 96.8 vs 321.9 ± 94.9 mmHg/s, P = 0.0017), and accordingly a wider gap between FG-PSP and FG-FFR (465.3 ± 119.4 vs 162.5 ± 123.6 mmHg/s, P = 0.0001) than DCM MA(−) patients. These characteristics of DCM MA(+) showed clear contrasts to those of the control patients. In conclusion, MA is caused with an impaired force-frequency relationship despite significant poststimulation potentiation, suggesting that MA reflects ineffective utilization of the potentiated intrinsic force during tachycardia. [ABSTRACT FROM AUTHOR]