Impact of neoadjuvant chemotherapy and chemoradiotherapy on postoperative cardiopulmonary complications in patients with esophageal cancer.

The effectiveness of neoadjuvant chemotherapy (nCT) or chemoradiotherapy (nCRT) for esophageal cancer patients is well established. However, neoadjuvant therapy may induce severe adverse effects that could increase postoperative morbidity. The current study evaluated the impacts of nCT and nCRT on postoperative cardiopulmonary complications in patient with esophageal cancer. We conducted a prospective study in esophageal cancer patients who received nCT (n = 126) or nCRT (n = 141) prior to surgery. Surgery was performed in all these patients following nCT or nCRT treatment. More patients occurred pneumonia in the nCRT-treated group compared with the nCT group (P < 0.01). The E-velocity (early diastolic filling velocity) decreased significantly (P = 0.026), while the N-terminal pro-brain natriuretic peptide (NT-proBNP) significantly increased (P < 0.01) in patients of the nCRT group compared with patients from the nCT group. Furthermore, a multivariate analysis revealed that nCRT was correlated with the incidence of pneumonia and NT-proBNP level significantly. The nCRT caused more cardiopulmonary toxicity than nCT. The strategies are needed to prevent the postoperative cardiopulmonary complications especially in patients with nCRT treatment.

A history of pulmonary embolism and deep venous thrombosis.

Although enormous progress has been made in understanding the physiology of pulmonary embolism, developing new diagnostic modalities and strategies, and constant refinement in the use of heparin therapy and thrombolytic therapy, venous thromboembolism remains a common and lethal process. As the history of this disease illustrates, advances continue to be made and it is anticipated that with newer diagnostic studies and anticoagulants under development, diagnosis and treatment of pulmonary embolism will continue to improve.

Rehabilitation for the home care patient with COPD.

Assessment techniques and treatment strategies, such as medical management, oxygen management, chest physical therapy, and pulmonary rehabilitation, for patients with chronic obstructive pulmonary disease (COPD) are discussed. Clinically appropriate, evidence-based rehabilitation programs for home care may help to reduce care costs, reduce the impact of this chronic disease on patients with COPD, and prevent emergent care and rehospitalization.

Antiremodeling effects of iloprost and the dual-selective phosphodiesterase 3/4 inhibitor tolafentrine in chronic experimental pulmonary hypertension.

Severe pulmonary hypertension is a disabling disease with high mortality. We investigated acute and chronic effects of iloprost, a long-acting prostacyclin analogue, and the dual-selective phosphodiesterase 3/4 inhibitor tolafentrine in monocrotaline-induced pulmonary hypertension in rats. Twenty-eight and 42 days after administration of the alkaloid, right ventricular systolic pressure increased from 25.8+/-2.0 to 62.9+/-3.4 and 70.5+/-7.4 mm Hg, with concomitant decline in cardiac index, central venous oxygen saturation, and arterial oxygenation. Marked right heart hypertrophy was demonstrated by the strongly elevated ratio of right ventricle/left ventricle plus septum weight, and massive thickening of the precapillary artery smooth muscle layer was shown histologically. Western blot analysis demonstrated increased levels of matrix metalloproteinases (MMPs) -2 and -9 and increased gelatinolytic activities in isolated pulmonary arteries. In these animals, both intravenous iloprost and tolafentrine displayed characteristic features of pulmonary vasodilators. When chronically infused from days 14 to 28, both agents significantly attenuated all monocrotaline-induced hemodynamic and gas exchange abnormalities as well as right heart hypertrophy. Full normalization of all variables including right ventricle size was achieved on combined administration of both agents during this period. This was also true for MMP-2 and MMP-9 expression and activity. Moreover, when iloprost plus tolafentrine was used for late therapeutic intervention, with infusion from days 28 to 42 after full establishment of severe pulmonary hypertension and cor pulmonale, hemodynamic, gas exchange, and cardiac and pulmonary vascular remodeling changes were significantly reversed. We conclude that the combined administration of iloprost and a dual-selective phosphodiesterase 3/4 inhibitor prevents and reverses the development of pulmonary hypertension and cor pulmonale in response to monocrotaline in rats. This regimen may therefore offer a possible antiremodeling therapy in severe pulmonary hypertension.

[Primary pulmonary hypertension]. / Primäre pulmonale Hypertonie.

In 1% of the patients with cor pulmonale the cause of the high pulmonary artery pressure remains unclear. The underlying severe and mostly progressive pulmonary vascular disease with unknown aetiology is defined as primary pulmonary hypertension (PPH) with three different pathomorphological subtypes, plexogenic pulmonary arteriopathy (PPA), thrombotic pulmonary arteriopathy (TPA) and pulmonary venoocclusive disease (PVOD). The endemic occurrence of PPH after the ingestion of anorexigenic drugs (aminorex fumarate) and toxic rapeseed oil lead to the hypothesis that PPH is a pulmonary vascular reaction to exogenous toxic agents on the base of a genetic disposition. The initial response could be an endothelial cell dysfunction leading to pathological proliferation of vascular smooth muscle cells, vasospasm and local disturbances of haemostasis. The derived therapeutic concepts with vasodilators (high dose calcium channel-blocking therapy, prostacyclin) and with anticoagulant drugs show some encouraging results. The lung and heart-lung transplantation have become real therapeutic options for the patients with PPH considering the mostly still very unfavourable prognosis of PPH.

Multifocal atrial tachycardia as a prognostic indicator in patients with severe chronic obstructive pulmonary disease requiring mechanical ventilation.

The records of 121 patients admitted to the Medical Intensive Care Unit (MICU) of Chang Gung Memorial Hospital with severe chronic obstructive pulmonary disease (COPD) requiring mechanical ventilation were reviewed retrospectively. Eighty-seven percent (20/23) of the patients with multifocal atrial tachycardia (MAT) expired during their ICU admission in contrast to 23.5% (23/98) of those without MAT. The only differences between these two groups were incidence of cor pulmonale, and right axis deviation, right bundle branch block, pulmonale P in electrocardiogram. MAT might be considered as a grave prognostic sign in patients with COPD severe enough to require mechanical ventilation.

[The use of hyperbaric oxygenation for the treatment of patients with pneumoconiosis and pulmonary heart failure]. / Primenenie giperbaricheskoi oksigenatsii dlia lecheniia bol'nykh pnevmokoniozom s legochno-serdechnoi nedostatochnost'iu.

Examination of 76 patients with pneumoconiosis (stage I) revealed that hyperbaric oxygenation is increasing the force of cardiac contractions, reduction of the general peripheral resistance and reduction of the lesser circulation hypertension. The therapeutic action of hyperbaric oxygenation is related to its ability to remove the sequels of oxygen.

[Nifedipine in the treatment of chronic cor pulmonale]. / Apport de la nifédipine dans le traitement du coeur pulmonaire chronique.

The effects of a single dose of nifedipine (20 mg sublingual) on the haemodynamics and parameters of tissue oxygenation were assessed by right heart catheterisation and oximetry of mixed arterial and venous blood in 24 patients with pulmonary hypertension secondary to severe chronic obstructive airways disease. The haemodynamic effects of 15 days' oral therapy (30 mg/day) were studied in 10 other patients. Significant improvement in right ventricular pump function (25 p. 100 increase in cardiac index. average reduction of 3 mmHg of right ventricular end diastolic pressure), and lowering of pulmonary hypertension (mean pulmonary artery pressures reduced by an average of 10 p. 100 and total pulmonary resistance by 25 p. 100) were observed after the single dose of nifedipine. This improvement was maintained after oral therapy for 15 days. The significant improvement of tissue oxygenation was reflected by an increase in oxygen transport (+ 24 p. 100), in the coefficient of delivered oxygen (+ 19 p. 100), in the oxygen partial pressure (+ 4 p. 100) and saturation (+ 3 p. 100) in the mixed venous blood. Arterial lactate concentrations fell by about 28 p. 100. In addition, a moderate fall in ppO2 and arterial saturation was observed due to a weak shunt effect which was more than compensated by the increase in cardiac output, and especially by the increase in the coefficient of relieved oxygen. These results show that nifedipine may be a valuable addition in the treatment of cor pulmonale secondary to chronic obstructive airways disease by improving right ventricular haemodynamics and pulmonary circulation and by increasing the quantity of oxygen delivered.

Nifedipine inhibits hypoxic pulmonary vasoconstriction during rest and exercise in patients with cystic fibrosis and cor pulmonale.

Nifedipine has recently been reported to reduce pulmonary artery pressure and pulmonary vascular resistance during rest and exercise in adult patients with hypoxic pulmonary hypertension from chronic obstructive pulmonary disease. To determine whether nifedipine reduces pulmonary vascular resistance in patients with cor pulmonale from cystic fibrosis (CF), we studied 2 patients with severe CF lung disease during rest and exercise while breathing room air or receiving low-flow oxygen therapy. Nifedipine markedly lowered pulmonary vascular resistance and improved cardiac index and pulmonary pressure-flow relationships during all treatment conditions. Nifedipine did not substantially change arterial PO2, except for a slight decrease during exercise while receiving low-flow oxygen. Nifedipine, however, markedly increased oxygen delivery during rest and exercise. Both patients noted improved exercise tolerance with chronic nifedipine therapy. Nifedipine may be a useful adjuvant to supplemental oxygen in the treatment of patients with CF and cor pulmonale.

Oral nifedipine in chronic cor pulmonale secondary to severe chronic obstructive pulmonary disease (COPD).

Hemodynamic effects of orally-administered nifedipine were evaluated in 12 patients with pulmonary hypertension secondary to severe COPD after short-term (30 and 60 minutes) treatment and then again in eight of these 12 patients after long-term (average 55 days) treatment. Pulmonary vascular resistance (PVR) decreased from 426 +/- 52 to 294 +/- 28 dynes.s.cm-5 (p less than 0.001) after therapy with 20 mg sublingual nifedipine (at 60 minutes). Cardiac index (CI) increased from 3.7 +/- 0.2 to 4.6 +/- 0.3 L/min/m2 (p less than 0.001). There was a decrease in mean pulmonary artery pressure (MPAP) only in 4/12 patients after Nifedipine. There was no significant fall in PaO2, while PvO2 and oxygen delivery (CI X CaO2) increased significantly 60 minutes after administration of sublingual nifedipine. PVR decreased from 482 +/- 82 to 374 +/- 44 dynes.s.cm-5 (p less than 0.05) after long-term nifedipine therapy. The changes in PVR and CI 60 minutes after administration of nifedipine in the patients on long-term treatment were similar to those observed with the same doses of nifedipine before initiation of therapy. Despite beneficial hemodynamic effects in two of eight patients, there was progressive clinical worsening. The benefit of long-term administration of nifedipine is difficult to predict on the basis of short-term effects.