**6. Mechanical circulatory support devices**

The prolonged use of dobutamine (7–52 days) is associated with much higher 6-month mortality

Milrinone is a noncatecholamine inotrope and peripheral vasodilator, has lusitropic effect and has less effect on HR than dobutamine. Milrinone works through the inhibition of phosphodiesterase enzymes (PDE), which in turn, leads to an increase in intracellular cyclic adenosine monophosphate (cAMP), which leads to an increase in the rate of entry and removal of calcium from the cardiac myocytes thus increasing myocardial contractility. Milrinone has been mainly used in the treatment of advanced severe heart failure patients, and—to date there have been head-to-head trials comparing dobutamine to milrinone. Milrinone should be

Levosimendan is a calcium-sensitizing agent that enhances myocardial inotropy and lusitropy and causes peripheral vasodilation, and it is not yet approved for use in the USA. Levosimendan is associated with similar mortality rates as compared to dobutamine but it tends to cause more peripheral vasodilation and hypotension than dobutamine [30, 39, 40].

Norepinephrine is preferred over dopamine as dopamine has been associated with a higher incidence of arrhythmias and a higher rate of death at 28 days in the CS patient subgroup [3]. In CS secondary to RV infarction, IV fluids are always the first line, but the excessive administration of IV fluids beyond an RA pressure of 15 mmHg could result in the deterioration of LV performance, and the use of dobutamine in this scenario can be particularly helpful in improving myocardial performance. Despite the severe hemodynamic compromise, arrhythmias, and increased in-hospital mortality, many patients with severe RV infarction recover within 3–10 days and typically, global RV function recovers within 3–12 months

Vasopressors and inotropes are essential in stabilizing CS patients but caution should always be taken with their use. The use of these agents causes an increase in the myocardial oxygen demand and can induce arrhythmias, and thus their use should always be individualized and guided by hemodynamic monitoring. The long-term use of inotropes is strongly discouraged, and should only be considered as a bridge to heart transplantation or ventricular assist

It is recommended to combine two small doses of vasopressors and inotropes than the use of a maximal dose of a single agent to avoid dose-related adverse events, also, the addition of vasopressin can help with "catecholamine sparing" [29]. The use of epinephrine in CS patients is associated with higher 90-day mortality independent of a prior cardiac arrest, and,

Our experience with these vasoactive agents in CS has been to initiate norepinephrine followed by an inotrope and then a stepwise approach in the addition of further vasopressors and/or inotropes in the setting of refractory shock. A concomitant shock etiology, such as

References [20, 29] provide further information about inotropes and their mechanism of

septic shock, should always be investigated as the choice of these agents might differ.

devices (VAD) or as a palliative therapy in advanced heart failure patients [20, 29].

thus, its use is discouraged unless it is a last resort medication [42].

avoided in advanced kidney disease patients as it is cleared renally [30, 37, 38].

[29, 30, 34–36].

150 Interventional Cardiology

[13, 29, 41].

action.

In certain patients with CS, hemodynamic stabilization might not be achieved despite aggressive pharmacotherapy and revascularization, as a result, percutaneous mechanical circulatory support (MCS) devices might be considered for temporary stabilization [43]. The optimal MCS device offers rapid hemodynamic stabilization along with a low complication rate. To date, no trial has shown mortality benefit with the use of these devices in CS patients.

#### **6.1. Intra-aortic balloon pump counterpulsation**

IABP counterpulsation is the most common form of percutaneous LV support. The original idea of counterpulsation started in the 1960s as an external counterpulsation device stimulating the hemidiaphragm around the distal thoracic aorta with each diastole. IABP is implanted percutaneously through either of the femoral arteries using a double lumen catheter that is 7.5–8 Fr and is placed in the thoracic aorta with its tip distal to the left subclavian artery take off, and its proximal portion above the renal vessels (**Figure 5**) [43, 44].

IABP is a form of internal counterpulsation and acts as an assisting circulatory support device that inflates during diastole and deflates during systole. Its main mechanism is by diastolic augmentation during inflation that contributes to the coronary, cerebral, and systemic circulation. The presystolic deflation lowers the impedance to systolic ejection and subsequently lowers the myocardial work and oxygen demand. IABP usually causes between 0.5 and 1.0

**Figure 5.** Intra-aortic balloon pump. The left panel shows the balloon inflation during diastole and the right panel shows the balloon deflation during systole. Reproduced with permission from Getinge.

L/min increase in the CO. IABP induces around 10% drop in SBP indicating proper systolic unloading, causes an increase in DBP which in turn improves the coronary perfusion and leads to a net increase in the mean arterial pressure (MAP). There is also an increase in the LV ejection fraction with IABP and a decrease in the LV end diastolic volume and pressure [44–47].

Despite all the hemodynamic advantages with IABP, studies have failed to show any mortality benefit with its use. The SHOCK II trial, which compared IABP vs. medical stabilization, showed no difference in mortality along with other variables such as time to hemodynamic stabilization, length of ICU stay, the dose and duration of catecholamines, and changes in renal function [6, 48].

Currently the main indication for IABP counterpulsation is CS refractory to pharmacotherapy; IABP is currently a class IIa indication for the treatment of CS complicating a STEMI in the American Heart Association/American College of Cardiology guidelines (AHA/ACC), while its routine use in CS is discouraged by the European Society of Cardiology [21, 49].

Other indications where IABP can help stabilize the patient include refractory heart failure, papillary muscle rupture or acute mitral regurgitation, ventricular septal rupture, refractory unstable angina, high-risk PCI or the inability to wean from cardiopulmonary bypass [44, 49, 50].

The absolute contraindications to IABP are significant aortic regurgitation and aortic dissection. Other relative exclusion criteria include: significant peripheral arterial disease (PAD) that precludes placement, severe coagulopathy, active infection, and cancer with metastasis [44].

The complication rate with IABP is rather rare with thrombocytopenia and fever being the most common (about 50% and 40% of patients, respectively). Other major complications include: major limb ischemia (0.9% of patients); severe access site bleeding (0.8%); amputation (0.1%); balloon leak (1%); and IABP-related mortality (0.05%). The main risk factors associated with IABP complications are female gender, PAD, small body surface area (BSA) (BSA < 1.65 m2 ), and advanced age (>75 years) [51, 52].

Due to the lack of data, the use of anticoagulation with IABP is variable among different centers. Most centers, like ours, use anticoagulation, but some will not, especially with 1:1 pumping [43].
