Effects of low-dose recombinant human brain natriuretic peptide on anterior myocardial infarction complicated by cardiogenic shock

Abstract INTRODUCTION: The mortality due to cardiogenic shock complicating acute myocardial infarction (AMI) is high even in patients with early revascularization. Infusion of low dose recombinant human brain natriuretic peptide (rhBNP) at the time of AMI is well tolerated and could improve cardiac function. OBJECTIVE: The objective of this study was to evaluate the hemodynamic effects of rhBNP in AMI patients revascularized by emergency percutaneous coronary intervention (PCI) who developed cardiogenic shock. METHODS: A total of 48 patients with acute ST segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock and whose hemodynamic status was improved following emergency PCI were enrolled. Patients were randomly assigned to rhBNP (n=25) and control (n=23) groups. In addition to standard therapy, study group individuals received rhBNP by continuous infusion at 0.005 µg kg−1 min−1 for 72 hours. RESULTS: Baseline characteristics, medications, and peak of cardiac troponin I (cTnI) were similar between both groups. rhBNP treatment resulted in consistently improved pulmonary capillary wedge pressure (PCWP) compared to the control group. Respectively, 7 and 9 patients died in experimental and control groups. No drug-related serious adverse events occurred in either group. CONCLUSION: When added to standard care in stable patients with cardiogenic shock complicating anterior STEMI, low dose rhBNP improves PCWP and is well tolerated.

Treatment of ethanol-induced acute pulmonary hypertension and right ventricular dysfunction in pigs, by sildenafil analogue (UK343-664) or nitroglycerin.

In patients at risk for sudden ethanol (ETOH) intravascular absorption, prompt treatment of pulmonary hypertension (PHTN) will minimise the risk of cardiovascular decompensation. We investigated the haemodynamic effects of intravenous ETOH and the pulmonary vasodilatory effects of a sildenafil analogue (UK343-664) and nitroglycerin (NTG) during ETOH-induced PHTN in pigs. We studied pulmonary and systemic haemodynamics, and right ventricular rate or time derivate of pressure rise during ventricular contraction ( =dP/dT), as an index of contractility, in 23 pigs. ETOH was infused at a rate of 50 mg/kg/min, titrated to achieve a twofold increase in mean pulmonary arterial pressure (MPAP), and then discontinued. The animals were randomised to receive an infusion of 2 ml/kg ( n = 7) normal saline, a 500-microg/kg bolus of UK343-664 ( n = 8), or NTG 1 microg/kg ( n = 8); each was given over 60 seconds. Following ETOH infusion, dP/dT decreased central venous pressure (CVP), and MPAP increased significantly, resulting in significantly increased pulmonary vascular resistance (PVR). Within 2 minutes after treatment with either drug, CVP, heart rate (HR), and the systemic vascular resistance-to-pulmonary vascular resistance (SVR/PVR) ratio returned to baseline. However, at that time, only in the UK343-664 group, MPAP and dP/dT partially recovered and were different from the respective values at PHTN stage. NTG and UK343-664 decreased PVR within 2 minutes, from 1241+/-579 and 1224+/-494 dyne . cm/sec 5 , which were threefold-to-fourfold increased baseline values, to 672+/-308 and 538+/-203 dyne . cm/sec 5 respectively. However, only in the UK343-664 group, changes from baseline PVR values after treatment were significant compared to the maximal change during target PHTN. Neither drug caused a significant change in SVR. In this model of ETOH-induced PHTN, both UK343-664 and NTG were effective pulmonary vasodilators with a high degree of selectivity. However, the changes from baseline values of PVR, and the partial recovery of systemic pressure and RV contractility compared to the maximal change during target PHTN, were significant only in the sildenafil analogue group.

Propranolol is effective in decreasing stress response due to airway manipulation and CO2 pneumoperitoneum in patients undergoing laparoscopic cholecystectomy.

PURPOSE: to study the effect of Propranolol on hemodynamic response due to airway manipulation and carbon dioxide pneumoperitoneum on laparoscopic cholecystectomy cases. METHODS: 63 patients undergoing laparoscopic cholecystectomy under general anaesthesia were randomly divided into 3 groups; group 1 received 1.0 mg of Propranolol, group 2 received 0.5 mg of Propranolol and group 3 received 1 ml saline 5 minutes before induction of anaesthesia. Haemodynamic parameters were recorded for every 5 minutes from basal to 5 minutes after extubation and analyzed. RESULTS: Balanced anaesthesia used in our set up is effective in decreasing stress response due to airway manipulation (laryngoscopy and endotracheal intubation) but not effective in that due to CO2 pneumoperitoneum. Propranolol 1 mg 5 minutes before anaesthesia is effective in decreasing stress response due to airway manipulation and CO2 pneumoperitoneum in these groups of patients. CONCLUSION: Propranolol effectively blunts the stress response due to CO2 pneumoperitoneum during laparoscopic cholecystectomy.

Effects of Electroacupuncture on Minimum Alveolar Concentration of Isoflurane and Cardiovascular System in Isoflurane Anesthetized Dogs

The effects of electroacupuncture (EA) on the minimum alveolar concentration (MAC) and on the cardiovascular system were evaluated with dogs under isoflurane anesthesia. Eight healthy male beagles were randomly assigned to six study groups (five heads/group) with washout intervals of 7 ~ 31 days between experiments for recovery and anesthetic clearance. MAC of isoflurane and cardiovascular parameters were determined after EA at nonacupoint and and at acupoints LI-4, SP-6, ST-36 and TH-8. Electroacupuncture for 30 minutes at LI-4, SP-6, ST-36 and TH-8 acupoints lowered the MAC of isoflurane by 17.5 +/- 3.1%, 21.3 +/- 8.0%, 20.5 +/- 8.2% and 15.6 +/- 3.1%, respectively (p < 0.05). However, electrical stimulation of nonacupoint did not induce a significant change in MAC of isoflurane. In the cardiovascular system, the ST-36 group did not induce any significant change in cardiovascular parameters. In the TH-8 group, the mean and diastolic arterial pressure and the systemic vascular resistance were decreased. In the LI-4 group, cardiac output and cardiac index decreased after EA. These results indicate that EA at LI-4, SP-6 and ST-36 have advantages in isoflurane anesthesia in terms of reducing the dose of anesthetics and minimizing cardiovascular side effects.

Short-term effects of atenolol in patients with dilated cardiomyopathy.

Dilated cardiomyopathy is a common cause of heart failure with systolic dysfunction. Medications used to treat this condition are usually for symptomatic relief. We studied the effect of atenolol in heart failure caused by dilated cardiomyopathy in a double blinded randomized fashion. There were 17 males and 5 females. All patients underwent right and left heart catheterization, coronary angiography, endomyocardial biopsy, exercise testing and doppler echocardiography. By 3 months, atenolol significantly reduced resting and exercise heart rate and pulmonary capillary wedge pressure. There was no difference in exercise capacity. We conclude from this study that atenolol improve hemodynamic condition in patients with dilated cardiomyopathy without improving exercise capacity during this short observation period.

Beneficial effects of long-term metoprolol therapy on cardiac haemodynamics in patients with mitral stenosis in sinus rhythm--a randomised clinical trial.

We conducted a placebo controlled randomised clinical trial to evaluate the effects of 6 months therapy with metoprolol on resting and exercise haemodynamics in 31 patients with isolated mitral stenosis in sinus rhythm. Twenty six of them (placebo n = 13, metoprolol n = 13) completed the study protocol. Their mean age was 23.1 +/- 7.9 years and the mean mitral valve area was 0.93 +/- 0.25 cm2. The dose of metoprolol ranged between 50-100 mg per day. The primary outcome variables for the study were the resting and exercise mean pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) and the secondary outcome variables consisted of resting and exercise heart rate, mean pulmonary artery pressure (PAP), mean pulmonary vascular resistance (PVR) and clinical improvement on visual analog scale. These outcome variables were assessed blindly. The resting and exercise mean PCWP (mmHg) increased by 9.1 +/- 3.1 and 16.4 +/- 6.4 on placebo and 2.5 +/- 2.1 and -4.6 +/- 2.3 on metoprolol after 6 months therapy. These differences were statistically significant (p < 0.01). The resting and exercise CI (liters/min/m2) decreased by 0.2 +/- 0.1 and 0.1 +/- 0.1 on placebo and 0.3 +/- 0.5 and 0.3 +/- 1.0 on metoprolol. These haemodynamic effects were accompanied with much better symptomatic improvement in patients treated with metoprolol. The differences in change in mean PAP and PVR in two groups were statistically not significant. Our results suggest that the symptomatic patients with MS, waiting for definitive intervention for 6 months or less, would benefit if given beta blockers during this period.

Lack of effect of nifedipine and pulmonary hypertension in a group of COPD decompensated patients

Se estudió el efecto del oxígeno y de la nifedipina (NFD) en la hemodinamia y el intercambio gaseoso en un grupo de 20 pacientes con enfermedad pulmonar obstructiva crónica. Los pacientes se encontraban respirando espontáneamente y fueron estudiados antes y después de recibir 30mg de NFD sublingual respirando aire u oxígeno (FIO20,40). No se encontraron cambios significativos de la presión media de la arteria pulmonar (PAP) con O2 o NFD. La resistencia vascular pulmonar (PVR) disminuyó solamente después de la administración de NFD. La presión wedge (PAPWd) y la presión auricular derecha (RAP) aumentaron con la NFD. La NFD produjo una pequeña pero significativa disminución de la PaO2 y aumento del Qva/Qt. Se encontraron correlaciones significativas entre los valores basales de PVR vs PaO2 y PvO2 (r=-0,51, p<0,02 y r=-0,63, p<0,01, respectivamente); Q vs Qva/Qt con aire o con O2 (r=0,58, p<0,01 y 0,48, p< 0,05, respectivamente); valores basales de saturación arterial de oxígeno vs cambio de la PVR producido por la NFD (r=0,65, p<0,01); Qva/Qt basal vs cambio del Qva/Qt luego de la NFD (deltaQva/Qt%) (r=0,78,p<0,01). En este grupo de pacientes la NFD no cambió la PAP, disminuyendo la PVR. La presion auricular derecha aumentó ligeramente y el trabajo ventricular derecho no cambió con la administración de NFD. Nosotros pensamos que estos dos hallazgos no son positivos en el manejo de pacientes con insuficiencia ventricular derecha. Por otro lado a NFD desmejoró ligeramente el intercambio gaseoso. Teniendo en cuenta que la NFD inhibe la vasoconstricción pulmonar hipóxica (HPV), la relación encontrada entre los valores de Qva/Qt basales y el deltaQva/Qt% producido por la NFD, demostraría que la HPV es más fuerte en aquelles pacientes descompensados que mantienen mejor intercambio gaseoso, y más débil en los que tienen peor intercambio gaseoso