Catheter-Directed Thrombectomy for Pulmonary Embolism in the Setting of Acute Stroke.

A 79-year-old male presented with an acute stroke and was treated with tissue plasminogen activator (tPA). His neurological symptoms improved, but he subsequently developed hemodynamic instability requiring intubation and vasopressors. Imaging studies revealed a massive pulmonary embolism as the cause of his worsening clinical picture. Mechanical thrombectomy using traditional devices was deemed too risky as the patient could not safely tolerate the usual anticoagulation dosage these devices require. The Penumbra Indigo® system (Alameda, CA, USA) was thus chosen for its ability to achieve thrombus aspiration within a lower therapeutic heparin range. Pulmonary artery aspiration thrombectomy was done using the device, and three days after the procedure, he was extubated and weaned completely off vasopressors. The therapy's efficacy despite the patient's unique life-threatening conditions demonstrates a novel application of the state-of-the-art pulmonary embolism treatment currently in research.

Rapid Surface Cooling by ThermoSuit System Dramatically Reduces Scar Size, Prevents Post-Infarction Adverse Left Ventricular Remodeling, and Improves Cardiac Function in Rats.

BACKGROUND: The long-term effects of transient hypothermia by the non-invasive ThermoSuit apparatus on myocardial infarct (MI) scar size, left ventricular (LV) remodeling, and LV function were assessed in rat MI model. METHODS AND RESULTS: Rats were randomized to normothermic or hypothermic groups (n=14 in each group) and subjected to 30 minutes coronary artery occlusion and 6 weeks of reperfusion. For hypothermia therapy, rats were placed into the ThermoSuit apparatus at 2 minutes after the onset of coronary artery occlusion, were taken out of the apparatus when the core body temperature reached 32°C (in ≈8 minutes), and were then allowed to rewarm. After 6 weeks of recovery, rats treated with hypothermia demonstrated markedly reduced scar size (expressed as % of left ventricular area: hypothermia, 6.5±1.1%; normothermia, 19.4±1.7%; P=1.3×10(-6)); and thicker anterior LV wall (hypothermia, 1.57±0.09 mm; normothermia, 1.07±0.05 mm; P=3.4×10(-5)); decreased postmortem left ventricular volume (hypothermia, 0.45±0.04 mL; normothermia, 0.6±0.03 mL; P=0.028); and better LV fractional shortening by echocardiography (hypothermia, 37.2±2.8%; normothermia, 18.9±2.3%; P=0.0002) and LV ejection fraction by LV contrast ventriculography (hypothermia, 66.8±2.3%; normothermia, 56.0±2.0%; P=0.0014). CONCLUSIONS: Rapid, transient non-invasive surface cooling with the ThermoSuit apparatus in the acute phase of MI decreased scar size by 66.5%, attenuated adverse post-infarct left ventricular dilation and remodeling, and improved cardiac function in the chronic phase of experimental MI.

Rapid Induction of Hypothermia by the ThermoSuit System Profoundly Reduces Infarct Size and Anatomic Zone of No Reflow Following Ischemia-Reperfusion in Rabbit and Rat Hearts.

INTRODUCTION: Although hypothermia reduces myocardial infarct size, noninvasive and rapid cooling methods are lacking. This study tests the effectiveness of a novel cooling apparatus on myocardial infarct size and no-reflow area in 2 models of coronary artery occlusion (CAO). METHODS AND RESULTS: Animals were randomized to normothermic (N) or hypothermic (H) groups after isolation of a proximal coronary artery. Animals were subjected to 30 minutes CAO and 3 hours reperfusion. In protocol 1 (rabbit, n = 8 per group), hypothermia was initiated, using the ThermoSuit apparatus (convective-immersion cooling), 5 minutes after the onset of CAO to a goal temperature of ∼32°C. In protocol 2 (rat, n = 5 per group), hypothermia was initiated 2 minutes after the onset of CAO to a goal temperature of ∼30°C. Goal temperature was reached in ∼20 minutes. In protocol 1, hypothermia caused an 82% reduction in infarct size as a percentage of the ischemic risk zone (N, 44% ± 5%; H; 8% ± 2%, P < 0.001) and an 89% reduction in the no-reflow area (N, 44% ± 4%; H, 5% ± 1%, P < 0.001). In protocol 2, hypothermia caused a 73% infarct size reduction (N, 51% ± 5%; H, 14% ± 6%, P < 0.01) and a 99% reduction in the no-reflow area (N, 33% ± 5%; H, 0.4% ± 0.3%, P < 0.01). CONCLUSION: The ThermoSuit device induced rapid hypothermia and limited infarct size and no reflow to the greatest extent ever observed in this laboratory with a single intervention.

Hypothermia in the setting of experimental acute myocardial infarction: a comprehensive review.

A door-to-balloon time of less than 90 minutes is the gold standard for reperfusion therapy to treat acute myocardial infarction (MI). Because 30-day mortality remains ∼ 10%, new methods must be cultivated to limit myocardial injury. Therapeutic hypothermia has long been experimentally used to attenuate myocardial necrosis during MI with promising results, but the treatment has yet to gain popularity among most clinicians. Hypothermia, in the basic science setting, has been achieved using many techniques. In our review, we examine past and current methods of inducing hypothermia, benefits and setbacks of such methods, current and future clinical trials, and potential mechanisms.

Delayed treatment with hypothermia protects against the no-reflow phenomenon despite failure to reduce infarct size.

BACKGROUND: Many studies have shown that when hypothermia is started after coronary artery reperfusion (CAR), it is ineffective at reducing necrosis. However, some suggest that hypothermia may preferentially reduce no-reflow. Our aim was to test the effects of hypothermia on no-reflow when initiated close to reperfusion and 30 minutes after reperfusion, times not associated with a protective effect on myocardial infarct size. METHODS AND RESULTS: Rabbits received 30 minutes coronary artery occlusion/3 hours CAR. In protocol 1, hearts were treated for 1 hour with topical hypothermia (myocardial temperature ≈32°C) initiated at 5 minutes before or 5 minutes after CAR, and the results were compared with a normothermic group. In protocol 2, hypothermia was delayed until 30 minutes after CAR and control hearts remained normothermic. In protocol 1, risk zones were similar and infarct size was not significantly reduced by hypothermia initiated close to CAR. However, the no-reflow defect was significantly reduced by 43% (5 minutes before CAR) and 38% (5 minutes after CAR) in hypothermic compared with normothermic hearts (P=0.004, ANOVA, P=ns between the 2 treated groups). In protocol 2, risk zones and infarct sizes were similar, but delayed hypothermia significantly reduced no-reflow in hypothermic hearts by 30% (55±6% of the necrotic region in hypothermia group versus 79±6% with normothermia, P=0.008). CONCLUSION: These studies suggest that treatment with hypothermia reduces no-reflow even when initiated too late to reduce infarct size and that the microvasculature is especially receptive to the protective properties of hypothermia and confirm that microvascular damage is in large part a form of true reperfusion injury.