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Aortic counterpulsation in cardiogenic shock during acute myocardial infarction Expert Rev. Cardiovasc. Ther. 12(7), 913–917 (2014)

Andrea Rognoni*1, Chiara Cavallino2, Alessandro Lupi1, Alessia Veia1, Roberta Rosso1, Francesco Rametta2 and Angelo Sante Bongo1 1 Coronary Care Unit and Catheterization Laboratory, “Maggiore della Carita`” Hospital, Corso Mazzini 18, 28100 Novara, Italy 2 Department of Cardiology, A.S.L. VC, Vercelli, Italy *Author for correspondence: Tel.: +39 0321 373 3563 Fax: +39 0321 373 3442 [email protected]

Intra-aortic balloon counterpulsation is the most widely used form of mechanical hemodynamic support in the setting of cardiogenic shock due to ST-segment elevation myocardial infarction (STEMI). Intra-aortic balloon pump (IABP) is also strongly recommended (class 1b) in the current European guidelines for treatment of STEMI. The evidence of a possible benefit of IABP in this setting is based mainly on registry data and a few randomized trials. Cardiogenic shock and subsequent death due to STEMI result from three factors: hemodynamic deterioration, occurrence of multiorgan dysfunction and systemic inflammatory response. IABP does not cause an immediate improvement in blood pressure, but the recent SHOCK II trial shows positive effects on multiorgan dysfunction. Some experimental and clinical studies have indicated that IABP results in hemodynamic benefits as a result of afterload reduction and diastolic augmentation with improvement of coronary perfusion. However, the effect on cardiac output is modest and may not be sufficient to reduce mortality. Furthermore we can say that the use of IABP before coronary revascularization in the setting of STEMI complicated with cardiogenic shock may make the interventional procedure safer by improving left ventricular unloading. The purpose of the present review is to clarify the state of the art on this topic. KEYWORDS: aortic counterpulsation • cardiac failure • cardiogenick shock • myocardial infarction • primary coronary intervention

After almost 50 years, intra-aortic balloon counterpulsation (intra-aortic balloon pump [IABP]) is the most widely used left ventricular assist device in a variety of indications. During the last century, assistance to the heart in parallel was tried using several techniques; Claus et al. [1] used an extracorporeal pump to draw blood from the aorta during cardiac systole, thus lowering resistance to the left ventricle and reinjected it during diastole. With the description of this technique, they introduced the principle of counterpulsation. For the first time, since the introduction of this method, the term counterpulsation was misleading; the devices were not pumping against the direction to the left ventricle but in series with the heart into the aorta at a different phase of the cardiac cycle. In other words, the method described required catheterization of one or both femoral arteries with large catheters and handling blood outside the body. After these first experiments, Mason Sones introduced the balloon catheter in patients informahealthcare.com

10.1586/14779072.2014.921116

with ventricular fibrillation following coronary arterial catheterization; angiography during pumping showed the displacement of blood from the aorta to the periphery [2]. The modern IABP device, which consists of a balloon mounted on a flexible catheter, was described by Moulopoulos et al. in 1962 [3]; the original description was a latex tube tied around a polyethylene catheter with side holes. Carbon dioxide was used to inflate the balloon regulated via a three-way solenoid valve; balloon inflation occurred for a predetermined duration and was timed using the R wave on the electrocardiogram. In 1967, Kantrowitz started using the balloon to wean patients from the heart–lung machine [4]. Nevertheless, at the present time, cardiogenic shock is the most common cause of death from acute myocardial infarction (MI). According to data from the SHOCK registry, the mortality from cardiogenic shock complicating acute MI is 50–80%. In addition, data indicate that anterior MI is the most common territory leading

 2014 Informa UK Ltd

ISSN 1477-9072

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Rognoni, Cavallino, Lupi et al.

to cardiogenic shock. In the SHOCK registry, 55% of infarctions were anterior [5]. Cardiogenic shock is diagnosed at the bedside by observing the clinical signs of end-organ hypoperfusion such as altered mental status, cool and mottled extremities and oliguria. The diagnosis is confirmed by demonstrating hemodynamic criteria consistent with myocardial dysfunction [6,7]. In the early 2000s, the American and European guidelines for the use of IABP for the treatment of cardiogenic shock were given a class IB [8,9]; however, evidence was based mainly on registry data, and there was a lack of adequately powered randomized trials. Sjauw et al. in 2009 published a meta-analysis including seven randomized trials (1009 patients) and nine cohort studies (10,529 patients); the pooled data of randomized studies did not support IABP in patients with high-risk STsegment elevation MI (STEMI). Instead, the data regarding cohort studies supported IABP therapy adjunctive to thrombolysis and not to primary percutaneous intervention (pPCI) in the setting of cardiogenic shock due to STEMI [4]. The IABP– SHOCK trial including only 45 patients showed no significant differences with respect to the severity of illness (using APACHE II score) between patients assigned to IABP and no IABP group [10]. In the SHOCK II trial and in the final 12 months follow-up study, Thiele et al. demonstrated that the use of IABP did not significantly reduce 30-day and 12-month all-cause mortality in patients with cardiogenic shock, complicating MI for whom pPCI was planned. The purpose of the present review is to make clear the state of the art for the use of IABP in the setting of cardiogenic shock due to acute MI [11,12]. The most recent and the latest American and European guidelines of management of STEMI downgraded the use of IABP, respectively, to IIa and IIb recommendation [13,14]. Pathophysiology & effects of aortic counterpulsation on systemic hemodynamics & coronary perfusion

The IABP improves many of the hemodynamic perturbations of circulatory failure and cardiogenic shock. Therefore, understanding the pathophysiology of this dramatic manifestation of heart failure is important. Cardiogenic shock is characterized by end-organ tissue hypoperfusion, which initiates a series of counterregulatory mechanisms. The classic understanding of the interplay between the underlying pathophysiology and counterregulatory mechanisms is that of a downward spiral in which compensatory mechanisms such as peripheral vasoconstriction, tachycardia and neurohormonal regulatory activation contribute to further worsening of left ventricular failure. The intra-aortic balloon, by inflating during diastole, displaces blood volume from the thoracic aorta. In systole, as the balloon rapidly deflates, this creates a dead space, effectively reducing after load for myocardial ejection and improving forward flow from the left ventricle. The net effect is to decrease systolic aortic pressure by as much as 20% and increase diastolic pressure [15]. In a multicenter trial of counterpulsation in cardiogenic shock, a mean 30 mm Hg increase in diastolic pressure was observed with no significant change in heart rate [11]. The net effect on myocardial mechanics is to decrease 914

myocardial oxygen consumption, increase cardiac output and lower peak left ventricular wall stress [16]. The magnitude of counterpulsation hemodynamic effect depends on several factors including the relation of balloon volume to aorta size, heart rate and rhythm and aortic compliance [17]. In addition, diastolic augmentation is most efficient the closer the balloon is to the aortic valve [18]. To minimize the risk of cerebral embolism, the ideal IABP position in modern practice is 1 or 2 cm distal to the origin of the left subclavian artery. The augmentation of diastolic pressure by counterpulsation should be transmitted to the epicardial coronary circulation, leading to an increase in myocardial perfusion. However, the data suggest that the degree of coronary artery stenosis and the state of coronary autoregulation causes significant variation in response to counterpulsation. Kimura et al. [18], using an anesthetized canine model, showed that diastolic forward flow in the left anterior descending artery increased by 12% during counterpulsation. However, with partial ligation of the left main to create a critical stenosis, the effect of counterpulsation to augment left anterior descending artery flow was completely abolished [18]. In human subjects, data regarding augmentation of coronary flow by counterpulsation are inconsistent. Transesophageal echocardiography Doppler tracings from epicardial vessels obtained in patients with an IABP have shown increased Doppler velocities, suggesting augmented coronary flow [19]. The effect of diastolic augmentation on poststenotic coronary flow has also been assessed using a Doppler angioplasty guidewire in patients undergoing angioplasty. Kern et al. studied coronary flow in 15 patients with a mean vessel narrowing of 95%. No significant increase in coronary flow augmentation was demonstrated in the poststenotic segment, but angioplasty restored the effect of counterpulsation to augment coronary flow [20]. Because of the severity of luminal obstruction present in the population studied, the use of a guidewire beyond the stenosis may have adversely affected flow measurements. In addition, conclusions cannot be drawn regarding flow augmentation beyond less severe stenoses, since these were not studied. Takeuchi et al. [21] addressed this issue by comparing 40 patients undergoing counterpulsation for typical indications using transthoracic Doppler echocardiography to measure coronary flow velocity. Analysis of the data stratified by lesion severity showed enhanced distal vessel flow regardless of the degree of stenosis present [4]. Nonetheless, a major contributor to the relief of ischemia by counterpulsation is via its effect to decrease after load, left ventricular wall stress and myocardial oxygen demand. Complications of IABP insertion

The Benchmark Counterpulsation Outcomes Registry published outcomes data on 16,909 patients undergoing IABP therapy between 1996 and 2000. The total incidence of major complications was 2.6%; incidence of minor complications was 4.2%. Specifically, the incidence of major limb ischemia, defined as loss of pulse, abnormal limb temperature or pallor requiring surgical intervention, was 0.9% [22]. The incidence of Expert Rev. Cardiovasc. Ther. 12(7), (2014)

Expert Review of Cardiovascular Therapy Downloaded from informahealthcare.com by Nyu Medical Center on 10/12/14 For personal use only.

Aortic counterpulsation in cardiogenic shock during acute MI

bleeding associated with hemodynamic compromise, requiring transfusion or surgical intervention, was 0.8%. In addition to vascular and bleeding complications, IABP may be associated with systemic cholesterol embolization, infection and stroke. The incidence of unsuccessful attempts at IABP placement recorded in the Benchmark Registry was low at 2.3% [22]. Complications attributed to device failure include balloon leak, balloon entrapment and poor balloon inflation. Shear forces created by the balloon can lead to hemolytic destruction of red cells and platelets; therefore, daily blood counts should be monitored during IABP therapy. In-hospital mortality attributed to IABP placement in the Benchmark Registry was 0.05%. The Benchmark Registry identified four risk factors for major complications from IABP use: age ‡75 years; female gender; peripheral arterial disease; body surface area

Aortic counterpulsation in cardiogenic shock during acute myocardial infarction.

Intra-aortic balloon counterpulsation is the most widely used form of mechanical hemodynamic support in the setting of cardiogenic shock due to ST-seg...
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