Pulmonary Embolism following Percutaneous Nephrolithotomy: An Uncommon and Life-Threatening Complication.

High risk pulmonary embolism is a rare and life-threatening complication following percutaneous nephrolithotomy. We report the case of a previously healthy, 44-year-old male, who developed acute pulmonary embolism following right percutaneous nephrolithotomy. On the 1st postoperative day, the patient presented with hemodynamic instability, acute respiratory distress, hypoxia, and loss of consciousness. He was urgently intubated and placed on mechanical ventilation. Clinical findings set the suspicion of pulmonary embolism with shock. Chest computed tomography scan confirmed the diagnosis. The patient underwent urgent thrombolysis in the cardiac care unit. On the 2nd postoperative day, the patient was admitted to the intensive care unit due to hemodynamic instability and fever. The postoperative course was complicated by right renal bleeding on the 3rd postoperative day, which was managed through angiography and angioembolization of the lower segmental right renal artery, followed by recurrent respiratory and urinary tract infections. The patient was transferred back to the urology department on the 66th postoperative day and was discharged seven days later.

Echocardiography and cardiac arrhythmias.

Cardiac arrhythmias refer to any abnormality or disturbance in the normal activation sequence of the myocardium and may be indicative of structural heart disease and the cause of significant cardiovascular complications and sudden cardiac death. The following review summarizes the current state-of-the-art knowledge on the role of echocardiography in the management of cardiac arrhythmias and focuses on atrial fibrillation and ventricular arrhythmias where echocardiography presents a particular diagnostic and prognostic interest. Moreover, a brief reference is made to the effect of cardiac arrhythmias and conduction abnormalities on echocardiographic examination.

Endothelin B-receptors and sympathetic activation: impact on ventricular arrhythmogenesis during acute myocardial infarction.

AIMS: We investigated the role of endothelin-B receptors on sympathetic activation originating from the adrenal gland or from the myocardium and its impact on arrhythmogenesis during acute myocardial infarction. MAIN METHODS: We studied two groups of rats (n=120, 284±2 g), namely wild-type and ETB-deficient. Myocardial infarction was induced by permanent ligation of the left coronary artery and ventricular tachyarrhythmias were evaluated from continuous electrocardiographic recordings. Sympathetic activation, measured by indices of heart rate variability, was evaluated after adrenalectomy or catecholamine depletion induced by reserpine. Acute left ventricular failure was assessed by total animal activity. KEY FINDINGS: Adrenalectomy decreased the total duration of tachyarrhythmias in ETB-deficient rats, but their incidence remained higher, compared to wild-type rats. After reserpine, heart rate variability indices and tachyarrhythmias were similar in the two groups during the initial, ischaemic phase. During evolving infarction, tachyarrhythmia duration was longer in ETB-deficient rats, despite lower sympathetic activation. Heart rate was lower in ETB-deficient rats throughout the 24-hour observation period, whereas activity was comparable in the two groups. SIGNIFICANCE: Endothelin-B receptors modulate sympathetic activation during acute myocardial infarction not only in the ventricular myocardium, but also in the adrenal gland. Sympathetic activation markedly increases early-phase ventricular tachyarrhythmias, but other mechanisms involving the endothelin system underlie delayed arrhythmogenesis.

Short-term ventricular restraint attenuates post-infarction remodeling in rats.

BACKGROUND/OBJECTIVES: Left ventricular restraint attenuates post-infarction remodeling, but may be associated with unfavorable long-term histological response. We hypothesized that beneficial effects can be obtained with short-term restraint during the early post-infarction period; for this purpose, we evaluated a biodegradable scaffold in the in vivo rat model and compared it with epicardial hydrogel application. METHODS: A total of 230 Wistar rats (358 ± 7 g) were studied. Implantation was performed with and without prior myocardial infarction, induced by permanent coronary artery ligation. Diastolic filling was evaluated by left ventricular pressure recordings after scaffold implantation. Degradation rates and inflammatory/foreign body response were studied at 3, 7 and 15 days post-ligation. Remodeling indices were evaluated by echocardiography 15 days post-ligation. RESULTS: No differences were found in diastolic pressure. Biodegradability was ~50% by 7 days and 100% by 15 days for both materials. Likewise, inflammatory/foreign body response peaked at 3 days post-implant, with subsequent remission, but fibroblastic reaction was more pronounced after scaffold than after hydrogel implantation. Post-ligation, ejection fraction was higher in the scaffold (40.0 ± 1.5%) or hydrogel groups (37.0 ± 1.3%), compared to controls (30.6 ± 1.9%). Wall tension index was lower with either biomaterial, but left ventricular end-diastolic diameter was shorter (p=0.044) and sphericity was attenuated (p=0.029) after scaffold, compared to hydrogel implantation. CONCLUSIONS: Both biomaterials showed a favorable histological response and attenuated remodeling, but epicardial restraint produced better results compared to hydrogel alone. The latter approach merits further investigation due to the ease of implantation.

Transforming growth factor-ß inhibition and endothelin receptor blockade in rats with monocrotaline-induced pulmonary hypertension.

Transforming growth factor-ß (TGF-ß) inhibition is an investigational therapy for pulmonary arterial hypertension with promising results in experimental studies. The present work compared this approach with endothelin-receptor blockade and evaluated the effects of combined administration. Pulmonary arterial hypertension was induced by single monocrotaline injection (60 mg/kg) in 75 Wistar rats and 15 rats served as controls. Intervention groups consisted of treatment with an antibody against TGF-ß-ligand, bosentan, both or none, initiated four weeks after monocrotaline injection. Right ventricular systolic pressure, pulmonary vascular remodeling, and exercise tolerance were evaluated eight weeks after monocrotaline injection. Either treatment, alone or in combination, lowered mortality. Comparable efficacy was found in the three treatment groups in terms of right ventricular systolic pressure (~45% decrease) and hypertrophy (~30% decrease), as well as exercise capacity. The three treatment groups equally ameliorated pulmonary vascular remodeling, evidenced by decreased vessel-wall thickness (in vessels 50-200 µm) and a smaller number of pre-capillary arterioles (< 50 µm) with a muscularized media. Treatment either with an antibody against TGF-ß or with endothelin receptor blockade are equally effective in experimental pulmonary hypertension. Their combination provides no added benefit, indicating common mechanisms of action.

Transforming growth factor-ß inhibition attenuates pulmonary arterial hypertension in rats.

The role of transforming growth factor-ß in the pathogenesis of pulmonary arterial hypertension is unclear. We examined the effects of T9429, an antibody against transforming growth factor-ß receptors, on hemodynamic, histological and functional parameters in the rat model of monocrotaline-induced pulmonary hypertension. One week after monocrotaline injection (60 mg/kg) in 28 Wistar rats, T9429 (0.1mg/kg daily) was administered intraperito-neally in 19 rats (268±10g) via an osmotic mini-pump for 7 days. One week thereafter, right ventricular systolic pressure, pulmonary vascular remodeling and exercise tolerance were evaluated. Compared to the monocrotaline group (25.5±1.9mmHg), right ventricular systolic pressure was lower (p=0.0014) in the monocrotaline+antibody group (18.4±0.8mmHg). This was translated into attenuated right ventricular hypertrophy (p=0.0063) and longer (p=0.0155) exercise duration (2.08±0.29min versus 6.19±1.02min). Pulmonary arterial wall thickness (in vessels 50 -200µm) was comparable between the two groups, but the monocrotaline+antibody group displayed lower number (p<0.0001) of pre-capillary arterioles (<50µm, in 20 randomly selected fields) with a muscularized media (23.33±3.15 versus 6.64±0.75). Our results suggest that transforming growth factor-ß receptor blockade improves vascular remodeling and attenuates pulmonary hypertension, a finding with potential therapeutic implications.

Do endothelin receptor antagonists have an antiarrhythmic potential during acute myocardial infarction? Evidence from experimental studies.

Sudden cardiac death constitutes a major health-related problem. In the majority of cases, sudden cardiac death is due to ventricular tachyarrhythmias secondary to acute myocardial infarction. The pathophysiologic chain of events leading to ventricular tachyarrhythmias after acute coronary occlusion is complex and incompletely understood. Experimental and clinical studies have indicated that endothelin-1 production rises markedly very early in the course of myocardial infarction. Endothelin-1 exerts significant electrophysiologic actions on ventricular cardiomyocytes and participates in the genesis of ischemic ventricular tachyarrhythmias. Endothelin-1, acting via two G-protein-coupled receptors (ETA and ETB), prolongs the action potential duration and increases the occurrence of spontaneous calcium transients, resulting in early afterdepolarizations and ventricular tachyarrhythmias via triggered activity. Moreover, endothelin-1 enhances sympathetic stimulation, a well established contributor to ventricular arrhythmogenesis during acute myocardial infarction. Despite these considerations, the therapeutic potential of endothelin receptor antagonists as antiarrhythmic drugs during myocardial ischemia/infarction is still under investigation. To date, a number of endothelin-1 receptor antagonists are available, presenting different degrees of selectivity for ETA and ETB receptors. The arrhythmogenic effects of endothelin-1 are exerted mainly via stimulation of the ETA receptors, but the role of ETB receptors remains controversial, as previous studies have produced conflicting results. This review summarizes the current state-of-the-art on the role of endothelin-1 in the genesis of ventricular arrhythmias during acute myocardial infarction and raises some hypotheses that could be explored in future studies.

Endothelin-B receptors and ventricular arrhythmogenesis in the rat model of acute myocardial infarction.

The arrhythmogenic effects of endothelin-1 (ET-1) are mediated via ETA-receptors, but the role of ETB-receptors is unclear. We examined the pathophysiologic role of ETB-receptors on ventricular tachyarrhythmias (VT/VF) during myocardial infarction (MI). MI was induced by coronary ligation in two animal groups, namely in wild-type (n = 63) and in ETB-receptor-deficient (n = 61) rats. Using a telemetry recorder, VT/VF episodes were evaluated during phase I (the 1st hour) and phase II (2-24 h) post-MI, with and without prior beta-blockade. Action potential duration at 90% repolarization (APD90) was measured from monophasic epicardial recordings and indices of sympathetic activation were assessed using fast-Fourier analysis of heart rate variability. Serum epinephrine and norepinephrine were measured with radioimmunoassay. MI size was similar in the two groups. There was a marked temporal variation in VT/VF duration; during phase I, it was higher (p = 0.0087) in ETB-deficient (1,519 +/- 421 s) than in wild-type (190 +/- 34 s) rats, but tended (p = 0.086) to be lower in ETB-deficient (4.2 +/- 2.0 s) than in wild-type (27.7 +/- 8.0 s) rats during phase II. Overall, the severity of VT/VF was greater in ETB-deficient rats, evidenced by higher (p = 0.0058) mortality (72.0% vs. 32.1%). There was a temporal variation in heart rate and in the ratio of low- to high-frequency spectra, being higher (<0.001) during phase I, but lower (p < 0.05) during phase II in ETB-deficient rats. Likewise, 1 h post-MI, serum epinephrine (p = 0.025) and norepinephrine (p < 0.0001) were higher in ETB-deficient (4.20 +/- 0.54, 14.24 +/- 1.39 ng/ml) than in wild-type (2.30 +/- 0.59, 5.26 +/- 0.67 ng/ml) rats, respectively. After beta-blockade, VT/VF episodes and mortality were similar in the two groups. The ETB-receptor decreases sympathetic activation and arrhythmogenesis during the early phase of MI, but these effects diminish during evolving MI.

[Right and left ventricular ejection fraction evaluation in patients with chronic pulmonary disease. Comparison of nuclear medicine methods].

UNLABELLED: Our aim was to evaluate right ventricular ejection fraction (RVEF) and left ventricular ejection fraction (LVEF) in patients with chronic pulmonary disease (CPD) during a standard 99mTc-isonitrilium myocardial perfusion study. Forty patients (14 women and 26 men, mean age 67.7 +/- 7 years old) suffering from CPD enrolled in this study. Patients were consecutively submitted to: a) First pass (FP) angiocardiography with 99mTc (Tauc-FP). b) Multigated angiocardiography (MUGA). c) FP with 99mTc-sestamibi (MIBI-FP). d) Gated FP (MIBI-gFP) and GatedSPECT was performed in 23 patients. A simple SPECT study was performed to the rest of them. Our results showed: For the RV: RVEF measured by each method: Tauc-FP =49.09+/-8.4%, MUGA =48.51+/-10.6%, MIBI-FP =49.45+/-7.8 % and MIBI-gFP =52.49+/-6.05%. No difference among these methods was noted (P=0.674). MIBI-FP ejection fraction range was wider than MIBI-gFP and narrower than MUGA. A strong correlation (r=0.88 P<0.01) and good agreement was found between MIBI-gFP and MIBI-FP. Less strong correlation was estimated between not only Tc-FP and MUGA (r=0.76 P<0.01) but MIBI-FP and MUGA (r=0.68 P<0.01) as well with no sufficient agreement. For the LV: LVEF was also measured by each method: Tauc-FP=61,1+/-8,5%, MUGA=61,2+/-10%, MIBI-FP=61,8+/-6%,EF GSPECT=60,2+/-7%. There was a strong correlation (r=0.87 P<0.01) with good agreement between Tauc-FP and MUGA. For all patients, correlation between MIBI-FP and GSPECT was weak (r=0.62 P<0.01) but ameliorated by the exclusion of 4 patients with small end diastolic volumes (EDV) (r=0.82 P<0.01). The correlation between MUGA and GSPECT got stronger (r=0.85 P<0.01) by the same exclusion. Finally, a strong correlation (r=0.81 P<0.01) with sufficient agreement was noted between MIBI-FP and MUGA. IN CONCLUSION: For the RV: simple or gated FP are reliable with good agreement methods of RVEF evaluation in patients with CPD that can easily be performed during every radionuclide isonitrilium myocardial perfusion study. MUGA is proved to be comparative to the FP estimation of RV EF. The gFP affords the narrowest range of RVEF calculated, allowing the more accurate functional identification of RV borders. For the LV: FP (with 99mTc or with sestamibi-99mTc) is a reliable method of LVEF measurement in patients with CPD when compared with MUGA. MuIotaBetaIota-FP can evaluate LVEF during a standard myocardial perfusion study with radionuclide isonitrilium. GSPECT-EF correlation with EF measured by MUGA or FP is strongly affected by EDV.