Novel Pacemaker Relocation Method for Radiotherapy Against Overlapping Lung Cancer.

We experienced a case of a patient with a history of pacemaker implantation who was found to have lung cancer just behind the pacemaker. She was an 80-year-old woman with a history of valve replacement, pacemaker implantation, and sarcoidosis. Computed tomography showed a ground-glass opacity of 1.

Association between changes in nutritional status and ability to perform activities of daily living in older patients with heart failure: A stratified analysis by frailty status.

Objectives: We aimed to determine the association between changes in nutritional status and the activities of daily living (ADL) at discharge, considering frailty status of older patients with heart failure (HF).

Methods: This study included 491 older inpatients with HF categorized into the following groups based on their clinical frailty scale (CFS) scores: low, intermediate, and high. Changes in nutritional status were assessed using the Controlling Nutritional Status score at admission and discharge.

Combination of low muscle strength and malnutrition is associated with longer length of hospital stay among older patients with heart failure.

Background: Muscle strength and nutritional status are associated with length of hospital stay (LOHS) in older patients with heart failure (HF).

Objectives: The purpose of the study was to examine the association of the combination of muscle strength and nutritional status on LOHS in older patients with HF.

Methods: This retrospective cohort study included 414 older inpatients with HF (men, 57.

What is the optimal nutritional assessment tool for predicting decline in the activity of daily living among older patients with heart failure?

The clinical importance of nutritional management in activities of daily living (ADL) among older inpatients with heart failure (HF) is greatly increasing. We determined the optimal nutritional assessment tool that can predict ADL decline among older inpatients with HF. We prospectively investigated 91 inpatients aged ≥ 65 years with HF in an acute hospital.

Continuous inhibition of poly(ADP-ribose) polymerase does not reduce reperfusion injury in isolated rat heart.

Poly(ADP-ribose) polymerase (PARP), an enzyme that is important to the regulation of nuclear function, is activated by DNA strand breakage. In massive DNA damage, PARP is overactivated, exhausting nicotinamide adenine dinucleotide and leading to cell death. Recent studies have succeeded in reducing cellular damage in ischemia/reperfusion by inhibiting PARP.

Malignant solitary fibrous tumor of the left ventricular epicardium.

Reports describing solitary fibrous tumors of the pericardium are rare. Surgical treatment was performed on a 49-year-old woman with a large pericardial mass. The mass was attached to the left ventricular wall with a broad stalk and was free of the parietal pericardium.

Severe, short-term food restriction improves cardiac function following ischemia/reperfusion in perfused rat hearts.

The purpose of this study was to clarify the characteristics of improved ischemic tolerance induced by severe, short-term food restriction in isolated, perfused rat hearts. Male Wistar (8 week-old) rats were given a food intake equivalent to a 70% reduction on the food intake of ad-libitum fed rats for 11 days (FR group and AL group, respectively). After this period, hearts were isolated and perfused in the Langendorff mode, and subjected to 20 min of global ischemia followed by 30 min of reperfusion.

Fasudil prevents KATP channel-induced improvement in postischemic functional recovery.

Whereas activation of ATP-dependent potassium (K(ATP)) channels greatly improves postischemic myocardial recovery, the final effector mechanism for K(ATP) channel-induced cardioprotection remains elusive. RhoA is a GTPase that regulates a variety of cellular processes known to be involved with K(ATP) channel cardioprotection. Our goal was to determine whether the activity of a key rhoA effector, rho kinase (ROCK), is required for K(ATP) channel-induced cardioprotection.