The effects of mild induced hypothermia on the myocardium: a systematic review

Abstract

SummaryMild induced hypothermia improves neurological outcome and reduces mortality among initially comatose survivors of out-of-hospital cardiac arrest. Similar pathological processes occur in the heart and the brain, namely ischaemia followed by reperfusion injury. Animal data indicate that mild induced hypothermia results in improved myocardial salvage, reduced infarct size, reduced left ventricular remodelling and better long-term left ventricular function. Several small human studies suggest that infarct size may be reduced by mild induced hypothermia, although this has not reached significance in any human study to date. There are variable reports of harm to the myocardium caused by mild induced hypothermia, including reduced myocardial contractility and cardiac output, electrocardiographic changes and arrhythmias, especially bradycardia. These harmful effects are reversible with rewarming. Most patients who have a cardiac arrest do not survive, and full neurological recovery occurs in only 6-23% [1]. In order to improve survival and reduce such neurological injury, guidelines have recently been published describing the post-cardiac arrest bundle of care: this includes early coronary reperfusion if appropriate (primary angioplasty or thrombolysis), haemodynamic optimisation, and control of ventilation, blood glucose, temperature and seizures [2,3].Therapeutic hypothermia has become established as a recognised intervention following cardiac arrest [2]. Two randomised controlled trials have shown improved neurological outcome and reduced mortality in adults who were therapeutically cooled following out-ofhospital ventricular fibrillation (VF) cardiac arrest, where the patient was comatose following initial resuscitation, and where cooling was initiated within minutes to hours [4,5]. The International Liaison Committee on Resuscitation has recommended that all unconscious adult patients with spontaneous circulation after out-of-hospital VF cardiac arrest should be cooled to 32-34°C for 12-24 h [6]. Such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest [6].Cardiac arrest is thought to cause neurological injury by several mechanisms, including perfusion failure leading to cerebral ischaemia, and reperfusion leading to re-oxygenation injury [7][8][9][10]. Therapeutic hypothermia is thought to attenuate both these processes. Firstly, hypothermia is thought to protect against many of the processes associated with reperfusion and re-oxygenation [14][15][16][17][18]. Secondly, hypothermia reduces the cerebral metabolic rate for oxygen (CMRO 2 ) [11], and may therefore provide protection from ongoing cerebral ischaemia [12,13].Similar pathological processes occur in the heart following cardiac arrest and ⁄ or acute myocardial infarction (AMI), including perfusion failure followed by reperfusion and re-oxygenation injury [19][20][21][22]. It has been suggested that mild induced hypothermia may also be beneficial to the myocardium in a similar way that it is neuroprotective to the brain [2...

Post Cardiac Arrest Syndrome

“…47 There is also evidence that TH may be beneficial to the heart in the postarrest period. Animal studies have shown improvement in myocardial function, myocardial salvage, and reduced infarct size in the setting of cardiac arrest or acute myocardial infarction with the use of TH.…”

The precision of PiCCO®measurements in hypothermic post‐cardiac arrest patients

“…Early arterial hypotension is common and is associated with increased in-hospital mortality [1,3,4]. It is characterised by hypovolaemia [5], reversible myocardial stunning [4][5][6] and excessive vasodilation [7,8].…”

Spontaneous Hypothermia Is Not Able to Completely Counteract Cardiac Arrest-Induced Mitochondrial Impairment in the Rat Heart

“…We do not challenge the protective potency of hypothermia. However, we would like to draw attention to several reports describing cardiac disadvantages even under hypothermic conditions in humans (for review [2]). The Vijlbrief group itself has demonstrated impairment of cardiomyocytes by elevated troponin I levels in neonates after perinatal asphyxia under hypothermic conditions.…”