Article, Cardiology

Use of inhaled nitric oxide in the treatment of right ventricular myocardial infarction

Case Report

Use of inhaled nitric oxide in the treatment of Right ventricular myocardial infarction?

Abstract

In 50% of acute left ventricular inferior-posterior wall myocardial infarction (MI), concomitant right ventricular MI (RVMI) has been reported, with a dramatic increased rate of mortality. We report the case of a woman with RVMI complicated by cardiogenic shock due to dissection of the right coronary artery. She was treated with liquid infusion, epinephrine, milrinone, and an intraaortic balloon pump, but clinical condition decreased. She was then intubated, and prolonged inhalation of nitric oxide (12-15 ppm) was added. Both clinical and hemodynamic parameters slowly improved with decrease of systemic (2513 +- 708 shifted to 1802 +- 369 dynes x s/cm5) and Pulmonary vascular resistance (365 +- 183 to 309 +- 80 dynes x s/cm5) and central venous pressure (fell from 13 +- 4 mm Hg to 6 +- 4 mm Hg) and improvement of cardiac index (from 2.2 +- 0.5 to 3 +- 0.3 L/min per square meter). Inhalation of nitric oxide (iNO) withdrawal on day 7 caused a significant rebound pulmonary hypertension with decrease of cardiac output. Inhalation of nitric oxide was then reinstituted until day 8 and was finally gradually withdrawn without major hemodynamic variations. The patient was weaned from the ventilator on day 9 and was stable clinically and hemodynamically.

Although current international recommendations con- cerning the use of iNO in adults seem to limit the use of iNO as a rescue treatment in patients with severe acute pulmonary Arterial hypertension and/or severe refractory arterial hypoxemia, beneficial effect of iNO in the RVMI seems to be strongly supported in the setting of car- diogenic shock.

The first demonstration that inhalation of nitric oxide (iNO) decreases pulmonary artery pressure in patients with pulmonary hypertension was in the mid-1980s [1,2]. The licensed indication of iNO is restricted to persistent pulmonary hypertension in neonates, with both idiopathic and postsurgical pulmonary hypertension in the setting of congenital heart disease. Inhalation of nitric oxide has

? Intensive care unit at Department of Cardiothoracic Vascular Anesthesia and Intensive Care, IRCCS Policlinico S. Donato, Milan, Italy.

been used for many years for the treatment of acute respiratory distress syndrome and pulmonary hypertension both in the operating room and in the intensive care unit [3-8]. It has been demonstrated in both human experiments

[9] and clinical studies that iNO causes a concentration- dependent and immediate selective pulmonary vasodilatation in the presence of pulmonary hypertension. Inhalation of nitric oxide has also been shown to promote vasorelaxation in ventilated regions of the lung, while redelivering pulmonary blood flow, and reducing intrapulmonary shunt. Inhalation of nitric oxide might benefit selected patients with severe acute Pulmonary arterial hypertension and/or severe Refractory hypoxemia. In addition, it seems to be a useful drug for patients with pulmonary hypertension undergoing Heart transplantation. However, it is believed that iNO may have other pulmonary and extrapulmonary effects that need to be investigated further. Some literature seems to support the use of iNO in patients with acute right ventricular (RV) failure due to myocardial infarction (MI). Here, we report the case of a woman affected by RVMI complicated by cardiogenic shock who was treated success- fully with iNO.

A 70-year-old female was admitted to the ED with acute chest pain. The 12-lead electrocardiogram revealed clear signs of inferior wall acute MI, and the patient was promptly taken to the catheterization laboratory. The coronary angiogram showed subocclusion of the right coronary artery that was treated by percutaneous transluminal angioplasty with the placement of 3 bare-metal stents (Fig. 1). The procedure was complicated by cardiogenic shock due to dissection of right coronary artery (Fig. 2). An intraaortic balloon pump was subsequently inserted, liquid and epinephrine infusion was started, and the patient was immediately taken to the intensive care unit.

An echocardiogram was then promptly performed, which showed the scenario of acute inferior MI involving right ventricle (tricuspid annular plane systolic excursion, 12 mm). Clinical condition gradually decreased. The blood gas analysis revealed metabolic acidosis, the patient became anuric, and atrial fibrillation with a medium-high ventricular rate was registered, and despite hemodynamic support

therapy, the patient clearly had cardiogenic shock.

Echocardiography showed progressive worsening of RV systolic function (tricuspid annular plane systolic excursion, 6 mm). Infusion of milrinone was started without effect. The

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473.e4 Case Report

resistance (365 +- 183 to 309 +- 80 dynes x s/cm5) and central venous pressure (fell from 13 +- 4 mm Hg to 6 +- 4 mm Hg). Wedge pressure remained stable, and cardiac index improved (from 2.2 +- 0.5 to 3 +- 0.3 L/min per square meter). The patient’s metabolic acidosis disappeared, with blood lactates dropping from a peak of 8 to 1.5 mmol/L, and urine output progressively recovered.

With this improvement, catecholamines were progres- sively withdrawn, and the intraaortic balloon pump was removed on day 6 of hospitalization. The iNO withdrawal on day 7 caused a decrease of cardiac output (systemic and pulmonary vascular resistance jumped to 3000 and 490 dynes x s/cm5, respectively, whereas cardiac index dropped to 2.1 L/min per square meter). Inhalation of nitric oxide was then reinstituted until day 8 and was finally gradually withdrawn without major hemodynamic variations. The patient was weaned from the ventilator on day 9 and was transferred out of the intensive care unit on day 10 of admission. A recent 6-month follow-up telephone call after her discharge confirms that she remains in good clinical

Fig. 1 Coronary angiogram showed subocclusion of the right coronary artery.

patient was then intubated, and iNO of 12 to 15 ppm was added to reduce the RV afterload as much as possible and improving cardiac output. A pulmonary artery catheter (Swan-Ganz) was inserted, where the pulmonary pressure read 21/17 mm Hg, and pulmonary capillary wedge pressure was 12 mm Hg.

Both clinically and hemodynamic parameters, gradually improved with decreased both systemic (2513 +- 708 shifted to 1802 +- 369 dynes x s/cm5) and pulmonary vascular

Fig. 2 Coronary angiogram: dissection of right coronary artery.

condition at home.

In 50% of acute left ventricular inferior-posterior wall MI, concomitant RVMI has been reported [10] and is often complicated by hemodynamic instability, low cardiac output, and cardiogenic shock. The treatment of RVMI consists of coronary reperfusion by primary angioplasty and intraaortic balloon pump insertion in the setting of cardiogenic shock, and fluid therapy to preserve preload and inotropic agents, such as catecholamines and phoshodiesterase inhibitors if necessary, but their use is limited by arrhythmias and the presence of hypotension [11-15]. Afterload reduction without systemic hypotension [16,17] is the rationale for the use of iNO in patients with acute RV heart failure due to MI. The iNO effect is limited in the pulmonary circulation, as it is quickly bound to hemoglobin and inactivated [18]. The iNO administration reduces endogenous NO production, and therefore, rapid withdrawal of iNO can cause, such as in our patient, a significant rebound pulmonary hypertension, but this can be avoided by gradual withdrawal [19].

Spalding et al [20] demonstrated that iNO decreased RV afterload in a porcine model of RV infarction. Inglessis et al

[21] reported Hemodynamic improvement in 13 patients with RVMI and cardiogenic shock in which iNO (80 ppm at fraction of inspired oxygen value of 0.90) for only 10 minutes improve hemodynamic function.

In our patient, we observed for the first time that prolonged iNO administration resulted in beneficial hemodynamic effects reflected by an increase of cardiac index. This improvement is related to reduced RV filling pressures and to better Peripheral perfusion as evidenced by the fall in lactic acid levels. Although current recommenda- tions concerning the use of iNO in adults seem to limit the use of iNO as a rescue treatment in patients with severe acute pulmonary arterial hypertension and/or severe refractory arterial hypoxemia [22], the beneficial effect of iNO in the setting of RVMI seems to be strongly supported

Case Report 473.e5

in the setting of cardiogenic shock if other ventricular assist device facilities are not available.

Valentina Valenti MD Second School of Medicine University of Rome Sapienza

S. Andrea Hospital

Rome, Italy E-mail address: [email protected]

Amisha J. Patel MD University of Michigan Ann Arbor, MI, USA

Sebastiano Sciarretta MD Second School of Medicine University of Rome Sapienza

S. Andrea Hospital

Rome, Italy

Hassan Kandil MD Fabrizio Bettini MD Andrea Ballotta MD

Department of Cardiothoracic Vascular Anesthesia and

Intensive Care IRCCS Policlinico S.Donato

Milan, Italy

doi:10.1016/j.ajem.2010.04.017

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