Inhaled nitric oxide versus sodium nitroprusside for preoperative evaluation of pulmonary hypertension in heart transplant candidates.

OBJECTIVE: The development of pulmonary hypertension before heart transplantation increases the risk for postoperative right ventricular failure. Reversibility of pulmonary vascular resistance (PVR), which indicates the feasibility of heart transplantation, can be tested with the use of intravenous vasodilators, such as sodium nitroprusside (NaNTP) or prostacyclin. However, the drawback of these drugs is the development of systemic hypotension. The aim of this study was to evaluate the safely and feasibility of inhaled nitric oxide (iNO) compared with sodium nitroprusside to test PVR reversibility, while avoiding systemic hypotension. MATERIALS AND METHODS: We included all patients who were affected by end stage heart failure undergoing evaluation for heart transplantation if they showed elevated PVR > 2.5 Wood units and mean pulmonary arterial pressure (mPAP) >25 mm Hg. The hemodynamic parameters measured by right heart catheterization were: systolic blood pressure (SBP), mPAP, pulmonary capillary wedge pressure, and cardiac index (CI). The following variables were derived: transpulmonary gradient (TPG) and PVR. All patients were tested by both iNO (20-40 ppm) and intravenous NaNTP, at increasing dosages which were titrated based on systemic pressure. We randomly assigned the order of administration of iNO and NaNTP. RESULTS: The 9 male candidates has an average age of 56 ± 4 years. Seven of the 9 (71%) had postischemic cardiomyopathy, and 2 had idiopathic cardiomyopathy. We observed a reduction of mPAP (32% and 14%), PVR (41% and 32%), TPG (20% and 26%), and SBP (17% and 5%) and an increase of CI with administration of NaNTP and iNO, respectively. CONCLUSIONS: We observed a reduction in PVR and mPAP with administration of either iNO and NaNTP. A better effect of NaNTP was attributed to reducted post-load of the left ventricle. However, the main advantage of iNO was the absence of systemic hypotension and its selectivity for pulmonary vascular system, as underscored by TPG reduction.

Extracorporeal membrane oxygenation rescue therapy in a case of portopulmonary hypertension during liver transplantation: a case report.

Portopulmonary hypertension has been reported in 2% to 9% of candidates for liver transplantation (OLT). If it is moderate to severe, it represents a contraindication to the procedure until pulmonary vasodilatative therapy has been optimized. We report the case of a 43-year-old man, scheduled for OLT due to alcoholic cirrhosis with hemosiderosis. His Model for End-Stage Liver Disease was 25 at that time. The preoperative evaluation showed a severe alteration of diffusion (pO2 68 mm Hg), without hepatopulmonary syndrome or portopulmonary hypertension (PPH) upon basal and dobutamine stress echocardiography. At the beginning of the OLT the hemodynamic profile showed mean pulmonary artery pressure (mPAP) 38 mm Hg, wedge pressure (WP) 19 mm Hg, cardiac output (CO) 9.1 L/min, pulmonary vascular resistance (PVR) 166 dyne s/cm(5), transpulmonary gradient (TPG) 19 mm Hg, which lead us to promptly initiate inhaled nitric oxide (iNO) and intravenous epoprostenol 2 to 5 ng/kg/min. Upon graft reperfusion the hemodynamic profile was: mPAP 47 mm Hg, WP 23 mm Hg, CO 14.2 L/min, PVR 135 dyne s/cm(5), TPG 24 mm Hg, and at the end of surgery, mPAP 39 mm Hg, WP 20 mm Hg, CO 10.6 L/min, PVR 123 dyne s/cm(5), TPG 19 mm Hg. On postoperative day (POD) 3, we observed severe worsening of PPH: mPAP 60 mm Hg, WP 10 mm Hg, CO 9.8 L/min, PVR 395 dyne s/cm(5), TPG 50 mm Hg even with maximal pulmonary vasodilatatory therapy (ambrisentan 5 mg, intravenous sildenafil 20 mg × 3 and epoprostenol 22 ng/kg/min, iNO). Severe acute respiratory distress syndrome (ARDS) was presents. Therefore we decided to begin veno-venous extracorporeal membrane oxygenation (v-v ECMO) to correct the hypoxic vasoconstriction. Subsequent weaning from inotropic support with iNO and epoprostenol was possible on POD 7 due to mPAP 42 mm Hg, WP 15 mm Hg, CO 7.9 L/min, PVR 273 dyne s/cm(5), and TPG 27 mm Hg. On POD 11 he was weaned from ECMO due to: mPAP 40 mm Hg, WP 16 mm Hg, CO 6.5 L/min, PVR 295 dyne s/cm(5) and TPG 24 mm Hg. The patient was extubated on POD 17. The cardiac catheterization 1 month after OLT showed: mPAP 28 mm Hg, WP 13 mm Hg, CO 5.4 L/min, PVR 220 dyne s/cm(5) and TPG 15 mm Hg. ECMO rescue therapy in this "extreme" case allowed us to correct hypoxemia responsible for worsening of pulmonary hypertension allowing time to reach the goal of vasodilatatory therapy.

Percutaneous aortic valve replacement in two cases at high surgical risk: procedural details and implications for patient selection.

The morbidity and mortality burden of heart valve disease is increasing in the developing world, especially among the elderly. Whereas surgery remains the standard of care in fit patients with degenerative aortic stenosis, percutaneous aortic valve replacement could become an effective alternative to surgery in selected higher risk patients. The authors report on two women with aortic stenosis, both at high surgical risk (an 81-year-old female with coronary artery and cerebro-vascular disease, and a 70-year-old female with end-stage cirrhosis), in whom percutaneous valve replacement was effectively performed by means of transfemoral access and retrograde CoreValve Re-valving System implantation. Two major post-procedural complications occurred, both effectively managed, in the second patient: a third degree atrio-ventricular block (requiring permanent pace-maker implantation) and bleeding from the right femoral artery access (requiring implantation of two covered stents and blood transfusion). Despite the increased baseline risk, both patients were discharged asymptomatic, the first twelve days and the other three weeks after admission. In the authors' experience percutaneous aortic valve replacement can be performed with reasonable safety in patient with severe aortic stenosis at high surgical risk.

Safety of coronary collateral stenting in a patient with acute coronary syndrome.

A protective role of the presence of collateral arteries, generating smaller infarcts, improved ventricular function, fewer future cardiovascular events, and improved survival following a myocardial ischemia has been described in numerous reports. However little is known about atherosclerotic disease of the collateral vessels, and the possibility to treat critical stenosis of these vessels has never been described. Therefore this report describes a unique case of percutaneous coronary intervention on a well developed yet atherosclerotic coronary collateral vessel triggering an acute coronary syndrome with hemodynamic instability. In the present case balloon angioplasty and stenting of the collateral vessel was safe and effective. Nonetheless, further studies are warranted.

Evolving standard in the treatment of coronary artery disease. Drug-eluting stents.

Coronary stent implantation is the predominant method of percutaneous coronary interventions (PCI). This is to be attributed to the ease of use beside the better short and long term clinical outcome as compared to balloon angioplasty. Nevertheless, improvements in operator skill and stent technology together with better use of adjunctive pharmacological therapy have contributed to the improvement in clinical outcome. However, the main limitation of coronary stenting is still represented by in-stent restenosis (ISR) with an estimated rate of 17-32%. Thus, compared to coronary bypass surgery, the major adverse cardiac events following stent implantation are still higher and mainly represented by the need for re-intervention. The advent of drug eluting stents (DES) has led the experts to predict that with DES there will be little or no difference between PCI and coronary bypass surgery in terms of long-term outcome leading to a further expansion of indications. The clinical trial programs of the 2 available DES for clinical use (sirolimus-eluting stent, SES - Cypher and paclitaxol-eluting stent - Taxus) have been able to demonstrate the safety and clinical efficacy of both. Nevertheless, off-label use in patients on high risk for restenosis confirmed these data. At least for SES as was demonstrated by 2 "real world" registries. Thus, the introduction of DES represents a remarkable evolution for new standards in coronary artery disease treatment and offers hope to those patients considered to be "high risk" such as diabetics, patients with ISR, diffuse disease in whom surgery was previously the only therapeutic option. This paper will discuss the main results of the clinical trial programs of the DES (mentioned above) available for clinical use in the present time and analyze technical and procedural aspects which could affect long term outcome.

Primary pulmonary hypertension.

Primary Pulmonary Hypertension (PPH) is a rare disease that progressively increases pulmonary arterial pressure and pulmonary vascular resistance to the point of right heart failure, in the absence of secondary causes of the disease. The following specific risk factors that can trigger PPH have been identified and examined: appetite depressant drugs, oral contraceptives and hyperuricaemia. Familial PPH transmitted by an incomplete penetrance dominant autosomic mechanism is responsible for about 6% of PPH cases. Recent research groups have identified the gene responsible for familial PPH. Since pulmonary vasoconstriction is the prime cause of PPH, vasodilation of the pulmonary arterial circulation system (using prostacyclin in the form of epoprostenol or iloprost) is the main aim of treatment.