Stabilisation of medically refractory ventricular arrhythmia by intra-aortic balloon counterpulsation

Fotopoulos, Grigorios; Mason, Maureen; Walker, S; Jepson, Nigel; Patel, Dyviang; Mitchell, Andrew; Ilsley, Charles; Paul, Vincent

doi:10.1136/hrt.82.1.96

Cited by 46 publications

(39 citation statements)

References 24 publications

(4 reference statements)

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“…These findings implicate SAC activation in promoting ventricular arrhythmias in cardiomyopathies with increased tension in ventricular wall and oxidative stress. This SAC-related mechanism may explain, at least in part, the clinical findings that reducing myocardial wall tension and oxygen demand by left ventricular offloading using intra-aortic balloon counterpulsation significantly reduced ventricular arrhythmias in patients with medically refractory ventricular arrhythmias (12).…”

Section: Discussionmentioning

confidence: 99%

Stretch-activated channel activation promotes early afterdepolarizations in rat ventricular myocytes under oxidative stress

Wang¹,

Joyner²,

Wagner³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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BH. Stretch-activated channel activation promotes early afterdepolarizations in rat ventricular myocytes under oxidative stress. Am J Physiol Heart Circ Physiol 296: H1227-H1235, 2009. First published March 13, 2009 doi:10.1152/ajpheart.00808.2008.-Mechanical stretch and oxidative stress have been shown to prolong action potential duration (APD) and produce early afterdepolarizations (EADs). Here, we developed a simulation model to study the role of stretch-activated channel (SAC) currents in triggering EADs in ventricular myocytes under oxidative stress. We adapted our coupling clamp circuit so that a model ionic current representing the actual SAC current was injected into ventricular myocytes and added as a real-time current. This current was calculated as ISAC ϭ GSAC ‫ء‬ (Vm Ϫ ESAC), where GSAC is the stretch-activated conductance, Vm is the membrane potential, and ESAC is the reversal potential. In rat ventricular myocytes, application of GSAC did not produce sustained automaticity or EADs, although turn-on of GSAC did produce some transient automaticity at high levels of GSAC. Exposure of myocytes to 100 M H2O2 induced significant APD prolongation and increase in intracellular Ca 2ϩ load and transient, but no EAD or sustained automaticity was generated in the absence of GSAC. However, the combination of GSAC and H2O2 consistently produced EADs at lower levels of GSAC (2.6 Ϯ 0.4 nS, n ϭ 14, P Ͻ 0.05). Pacing myocytes at a faster rate further prolonged APD and promoted the development of EADs. SAC activation plays an important role in facilitating the development of EADs in ventricular myocytes under acute oxidative stress. This mechanism may contribute to the increased propensity to lethal ventricular arrhythmias seen in cardiomyopathies, where the myocardium stretch and oxidative stress generally coexist. arrhythmia mechanisms; action potential; patch clamp PREVIOUS STUDIES HAVE SHOWN that myocardial stretch, a process termed "mechanoelectric feedback," can induce myocyte depolarization and abnormal impulses by the stretch-activated channel (SAC) currents (7,21). A subset of SACs has been reported as nonselective cation channels (48), which allow Na ϩ , K ϩ , Cs ϩ , and Ca 2ϩ to permeate (36). A linear currentvoltage relationship has been described for SACs with reversal potentials measured in myocytes from Ϫ6 to Ϫ15 mV (17,33,48). In a review by Kohl et al. (24), they note that models incorporating SACs as pure charge carriers and models that include movement of ions through the channels both reproduced experimental phenomena, such as diastolic depolarization, positive chronotropic responses of pacemakers, and action potential (AP) generation due to stretch (25).It has been suggested that oxidative stress is a mechanism for Ca 2ϩ overload and the consequent electrical changes in cardiomyocytes (5). On the other hand, Ca 2ϩ overload increases oxidative stress by altering mitochondrial function, which leads to increased production of oxygen radicals (9). Oxidative stress alters the function of several elem...

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Section: Discussionmentioning

confidence: 99%

Stretch-activated channel activation promotes early afterdepolarizations in rat ventricular myocytes under oxidative stress

Wang¹,

Joyner²,

Wagner³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…There are 2 parts: a flexible catheter with 2 lumens (1 for pressure monitoring and 1 for gas exchange in the balloon), as well as a mobile console for the helium transfer system. This is useful during cardiogenic shock, 21 acute MI, 22 post-MI complications, refractory myocardial ischemia, 23 high-risk surgery, refractory ventricular arrhythmias, 24 and high-risk percutaneous intervention. 22, 25 Contraindications include aortic insufficiency, aortic dissections, and aorto-iliac vascular disease.…”

Section: Aortic Counterpulsationmentioning

confidence: 99%

Devices in Heart Failure

Gafoor

Franke

Lam

et al. 2015

Circ J

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“…Treatment of malignant arrhythmias may be an indication for implantation of an intraaortic balloon pump or other mechanical circulatory support (6,7). This may improve coronary perfusion, reduce the peripheral arterial resistance (afterload) and also reduce the need for proarrhythmic adrenergic agents.…”

Section: After Sedation and The Start Of Respirator Treatment The Simentioning

confidence: 99%

En mann i 50-årene med elektrisk storm etter hjerteinfarkt

Ross¹,

Rossvoll²,

Moufack³

et al. 2013

Tidsskriftet

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A man in his 50s without a previous history of heart disease was hospitalised with acute myocardial infarction. The course was complicated and required sophisticated treatment. Myocardial infarction with ST elevation in the ECG is almost always due to thrombotic occlusion of an epicardial coronary artery. In cases of myocardial infarction with ST elevation (STEMI), primary treatment is aimed at as rapid reperfusion as possible. This can be achieved by thrombolysis or by primary percutaneous coronary intervention (primary PCI). The time taken to reach the nearest PCI centre determines which treatment is chosen. If primary PCI cannot be performed within 120 minutes, thrombolysis is recommended (1). In the event of extensive ECG changes and a short history of illness, defined as < 2 hours, this time limit is shortened to 90 minutes (1).The regression of pain and ECG changes is a sign of successful thrombolysis, and a more than 50 % reduction of the ST elevation in the lead where this was most pronounced implies reperfusion (1). If there are no signs of reperfusion after 45 -60 minutes, rescue PCI is indicated. Approximately 30 % of those who undergo thrombolysis will need this (2). Rescue PCI was clearly indicated for our patient. The ECG showed persistent ST elevation and the recurrent ventricular arrhythmia strengthened suspicions of ongoing ischaemia. On arrival at the university hospital, the patient was taken immediately to the angiography laboratory. A coronary angiogram showed three-vessel disease with stenosis proximally in the anterior descending branch of the left coronary artery (LAD), stenosis in a marginal branch of the circumflex branch and several stenoses in the right coronary artery (Fig. 1). The LAD stenosis was considered to be the culprit lesion, and PCI was performed with implantation of a conventional metal stent -with a favourable angiographic result.In addition to stenosis in the LAD, which had probably caused the infarction, the patient had extensive coronary disease. However, it is not recommended that lesions other than the culprit lesion be treated in the acute phase (1). If there is an indication for treating other stenoses, this should be done later. The exception is in the case of cardiogenic shock, where efforts are made to achieve as complete revascularisation as possible already in the acute phase (1). An echocardiogram taken immediately on

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Stabilisation of medically refractory ventricular arrhythmia by intra-aortic balloon counterpulsation

Cited by 46 publications

References 24 publications

Stretch-activated channel activation promotes early afterdepolarizations in rat ventricular myocytes under oxidative stress

Stretch-activated channel activation promotes early afterdepolarizations in rat ventricular myocytes under oxidative stress

Devices in Heart Failure

En mann i 50-årene med elektrisk storm etter hjerteinfarkt

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