Slow ventricular tachycardia in a 91-year-old man with implantable cardioverter-defibrillator and acute respiratory failure.

Slow ventricular tachycardia (VT) in patients with devices such as an implantable cardioverter - defibrillator (ICD) is more common than in the rest of the population. The incidence in elderly patients with an ICD remains largely unknown. In younger patients, slow VT is generally asymptomatic or associated with limited clinical relevance. It may be efficiently and safely terminated by anti-tachycardia pacing. We present a case of slow VT in a 91-year-old man with ICD with type 1 acute respiratory failure and drowsiness. Very elderly patients who have poor cardiac reserve and minor deterioration in cardiac function can face serious consequences such as ventricular fibrillation, cardiac arrest, and sudden cardiac death. The persistent ventricular rhythm may have a deleterious effect on their haemodynamic status, with potential aggravation of symptoms of heart failure and further impairment of ventricular function.

Caring for critically ill oldest old patients: a clinical review.

Despite technological advances, the mortality rate for critically ill oldest old patients remains high. The intensive caring should be able to combine technology and a deep humanity considering that the patients are living the last part of their lives. In addition to the traditional goals of ICU of reducing morbidity and mortality, of maintaining organ functions and restoring health, caring for seriously oldest old patients should take into account their end-of-life preferences, the advance or proxy directives if available, the prognosis, the communication, their life expectancy and the impact of multimorbidity. The aim of this review was to focus on all these aspects with an emphasis on some intensive procedures such as mechanical ventilation, noninvasive mechanical ventilation, cardiopulmonary resuscitation, renal replacement therapy, hemodynamic support, evaluation of delirium and malnutrition in this heterogeneous frail ICU population.

Long-term mortality in frail elderly subjects with osteoarthritis.

OBJECTIVE: Elderly subjects are characterized by a high prevalence of OA and clinical frailty. This study aimed to examine the predictive role of clinical frailty on long-term mortality in elderly subjects with and without OA. METHODS: Mortality was evaluated after a 12-year follow-up in 698 subjects with and 590 subjects without OA recruited in 1992. Clinical frailty was assessed according to the Frailty Staging System and stratified in tertiles. RESULTS: After a 12-year follow-up, mortality was 42.2% in subjects without and 55.8% in subjects with OA (P = 0.256). With increasing frailty, mortality increased by 30.5% (P for trend < 0.001) in subjects without and by 45.6% in subjects with OA (P for trend < 0.001). Multivariate analysis showed that frailty [hazard ratio (HR) = 1.49 for each unit of increase, 95% CI 1.32, 1.94, P < 0.001) but not OA (HR = 1.28, 95% CI 0.987, 1.39, P = 0.412) was predictive of long-term mortality. Moreover, when Cox regression analysis was performed, frailty enhanced the risk of long-term mortality for each unit of increase by 32% (HR = 1.32, 95% CI 1.06, 1.65, P = 0.03) in the absence of OA and by 98% in the presence (HR = 1.98, 95% CI 1.63, 2.95, P < 0.01) of OA. CONCLUSION: Clinical frailty significantly predicts mortality in subjects without OA and even more in those with OA. Thus clinical frailty may be considered a new prognostic factor to identify subjects with OA at high risk of mortality.

Age-related reduction of cerebral ischemic preconditioning: myth or reality?

Stroke is one of the leading causes of death in industrialized countries for people older than 65 years of age. The reasons are still unclear. A reduction of endogenous mechanisms against ischemic insults has been proposed to explain this phenomenon. The "cerebral" ischemic preconditioning mechanism is characterized by a brief episode of ischemia that renders the brain more resistant against subsequent longer ischemic events. This ischemic tolerance has been shown in numerous experimental models of cerebral ischemia. This protective mechanism seems to be reduced with aging both in experimental and clinical studies. Alterations of mediators released and/or intracellular pathways may be responsible for age-related ischemic preconditioning reduction. Agents able to mimic the "cerebral" preconditioning effect may represent a new powerful tool for the treatment of acute ischemic stroke in the elderly. In this article, animal and human cerebral ischemic preconditioning, its age-related difference, and its potential therapeutical applications are discussed.