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Impact of pulmonary hypertension on lung cancer management
Abstract
Introduction
The diagnosis and management of lung cancer is challenging among patients followed-up for pulmonary hypertension (PH). Many interventional procedures are not suitable for severely ill patients, thus limiting the diagnosis and treatment of cancer. We report on patients diagnosed with both conditions in our Institution.
Methods
We conducted a retrospective observational cohort study at Toulouse University Hospital. We analysed both management and outcome for patients followed-up for precapillary PH following diagnosis of primary lung cancer.
Results
Out of 764 patients followed-up for PH, 25 went on to develop bronchopulmonary neoplasia. The median age was 69 years with a predominance of males (56%) and smokers (92%). Fifty-two percent had group 1 PH and 36% severe group 3 PH. The comorbidity burden was high and 76% were oxygen-dependent. Twenty-eight percent of patients were considered ineligible for tissue biopsy, the diagnosis being made by a multidisciplinary team (MDT) based on radio-clinical presentation. Fifty-four percent of patients did not benefit from any treatment. Sixteen percent of pulmonary diagnostic procedures were associated with complications (severe hypoxaemia, intra-alveolar hemorrhage, haemothorax). Patients were undertreated compared to disease stage guidelines (2 surgical procedures for 9 localised stages). Median survival after cancer diagnosis was 6 months.
Conclusion
The management of lung cancer is complex in PH patients. The high rate of complications during the diagnosis and therapy steps coupled with very poor patient outcome for both conditions should prompt physicians to thoroughly discuss the benefit/risk benefit in each case.
... PH in NSCLC may arise from shared risk factors, lung cancer itself, or cancer treatments. Emerging evidence links PH in NSCLC to vascular remodeling, inflammatory cell accumulation, and pulmonary tumor thrombotic microangiopathy, which can hinder cancer treatment and cause delays in care [41,43]. ...
Purpose
To identify non-cancerous factors from baseline CT chest affecting survival in advanced non-small cell lung cancer (NSCLC) treated with first-generation Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors (EGFR-TKIs).
Methods
Retrospective study of 172 advanced NSCLC patients treated with first-generation EGFR-TKIs as a first-line systemic treatment (January 2012 to September 2022). Baseline CT chest assessed visceral/subcutaneous fat (L1 level), sarcopenia, and myosteatosis (multiple levels), main pulmonary artery (MPA) size, MPA to aorta ratio, emphysema, and bone mineral density. Cox regression analyzed prognostic factors at 18-month outcome.
Results
Median overall survival was 17.57 months (14.87–20.10) with 76 (44.19%) patients died at 18 months. Deceased had lower baseline BMI (21.10 ± 3.44) vs. survived (23.25 ± 4.45) (p < 0.001). Univariable analysis showed 5 significant prognostic factors: low total adiposity with/without cutoff [HR 2.65 (1.68–4.18), p < 0.001; 1.00 (0.99–1.00), p = 0.006;], low subcutaneous adipose tissue (SAT) with/without cutoff [HR 1.95 (1.23–3.11), p = 0.005; 0.99 (0.98–0.99), p = 0.005], low SAT index (SATI) with/without cutoff [1.74 (1.10–2.78), p = 0.019; 0.98 (0.97–0.99), p = 0.003], high VSR [1.67 (1.06–2.62), p = 0.026], and high MPA size with/without cutoff [2.23 (1.23–4.04), p = 0.005; 1.09 (1.04–1.16), p = 0.001]. MPA size, MPA size > 29 mm, and total adiposity ≤85 cm² remained significant in multivariable analysis, adjusted by BMI [HR 1.14 (1.07–1.21), p < 0.001; 3.10 (1.81–5.28), p < 0.001; 3.91 (1.63–9.40), p = 0.002]. There was no significant difference of sarcopenic and myosteatotic parameters between the two groups.
Conclusion
In advanced EGFR-mutated NSCLC patients, assessing pre-treatment prognosis is warranted to predict the survival outcome and guide decision regarding EGFR-TKI therapy. Enlarged MPA size, low total adiposity, and low subcutaneous fat (lower SAT, lower SATI, and higher VSR) are indicators of poor survival. Large MPA size (>29 mm) or low total adiposity (≤85 cm²) alone predict 18-month death.
... The pulmonary arterial hypertension (PAH) dataset stood out for the large number of dysregulated genes [6], much higher than lung cancer [6,12], which made it more likely to find an important number of common DEGs with lung cancer. Pulmonary arterial hypertension (PAH) is the increase in mean pressure greater than 20 mmHg, found by right heart catheterization, which is associated with the lower survival of patients with lung cancer, since it increases the rate of complications during diagnosis and the treatment [10,27]. PAH is a very complex disease similar to cancer, with an important effect of environmental stress in its etiology, such as inflammation and hypoxia, which induce the formation of hyperproliferative and apoptotic-resistant clones of different cells involved in lung tissue, which in turn influence the development of PAH-affected cells that exhibit several hallmarks of cancer [26]. ...
The transcriptomic analysis of microarray and RNA-Seq datasets followed our own bioinformatic pipeline to identify a transcriptional regulatory network of lung cancer. Twenty-six transcription factors are dysregulated and co-expressed in most of the lung cancer and pulmonary arterial hypertension datasets, which makes them the most frequently dysregulated transcription factors. Co-expression, gene regulatory, coregulatory, and transcriptional regulatory networks, along with fibration symmetries, were constructed to identify common connection patterns, alignments, main regulators, and target genes in order to analyze transcription factor complex formation, as well as its synchronized co-expression patterns in every type of lung cancer. The regulatory function of the most frequently dysregulated transcription factors over lung cancer deregulated genes was validated with ChEA3 enrichment analysis. A Kaplan–Meier plotter analysis linked the dysregulation of the top transcription factors with lung cancer patients’ survival. Our results indicate that lung cancer has unique and common deregulated genes and transcription factors with pulmonary arterial hypertension, co-expressed and regulated in a coordinated and cooperative manner by the transcriptional regulatory network that might be associated with critical biological processes and signaling pathways related to the acquisition of the hallmarks of cancer, making them potentially relevant tumor biomarkers for lung cancer early diagnosis and targets for the development of personalized therapies against lung cancer.
IntroductionCardiovascular diseases present a great burden for survivors of hematologic malignancy (HM). However, the effect of pulmonary hypertension (PH) on the clinical outcome of patients with HM remains unknown. This study aims to evaluate the prognostic potential of PH in patients with HM and explore the related clinical determinants.Methods
This retrospective study included 220 patients with HM and PH and 220 controls without PH, the case-matching cohort analysis was performed based on age, sex, the year of diagnosis and disease type. The baseline characteristics and overall survival (OS) of the patients with HM with or without PH were compared. The cumulative overall survival was analyzed using the Kaplan–Meier curves and the log-rank test. Multivariate Cox proportional hazard models were conducted to identify the predictors of OS.ResultsPH was found in 11.98% (302/2520) of the patients with HM. The PH group had lower levels of hemoglobin, platelet, albumin, fibrinogen and B cell count; whereas the levels of lactate dehydrogenase, N terminal pro B type natriuretic peptide, d-dimer, fibrinogen degradation products and C-reactive protein were higher. Additionally, the PH group had a higher prevalence of atrial fibrillation. Survival analysis revealed that the PH group had an inferior OS compared to the non-PH group (16.9 vs. 37.6 months, p = 0.002). Further subgroup analysis revealed that the severe PH group had the worst OS, followed by the moderate and the mild PH groups (8.7 vs. 14.7 vs. 23.7 months, p < 0.001). Multivariate analysis showed that PH was an independent predictor for unfavorable clinical outcomes.Conclusions
Coexisting PH was associated with inferior clinical outcomes in patients with HM, and the severe PH group had the worst prognosis. The study may provide additional risk stratification for patients with HM.
Purpose
Pulmonary hypertension (PH) is an important comorbidity of lung cancer, PH in lung cancer patients is gradually gaining interest because of its apparent high prevalence, but the impact of PH on the outcomes of lung cancer remains uncertain and had rarely been discussed. We aimed to evaluate the prevalence, determinants and prognosis value of elevated pulmonary artery systolic pressure (PASP) in non-small cell lung cancer patients.
Patients and Methods
In this retrospective study, subjects with a new and pathological confirmed diagnosis of lung cancer were enrolled. All patients underwent transthoracic echocardiography before received treatment. Pulmonary artery systolic pressure was measured by transthoracic echocardiography. Lung cancer subtypes were categorized by WHO classification of lung tumors. Hazard ratios (HR) were estimated by using Cox regression models.
Results
Among 612 non-small cell lung cancer (NSCLC) patients, 19.8% coexisted with PH. After adjustment for age, symptom, coagulation disorders, lymph node metastasis, distant metastasis, histological type, clinical stage, PASP ≥35mmHg was significantly associated with the decreased overall survival (OS) of NSCLC (P= 0.028). Moreover, PASP ≥45mmHg was an independent predictor for perioperative death. Independent factors of comorbid elevated PASP were age, the presence of intrapulmonary metastasis and coagulation disorders.
Conclusion
These findings suggest that PASP is an independent prognostic risk factor for NSCLC patients. Main determinants of elevated PASP are age, the presence of intrapulmonary metastasis and coagulation disorders.
Background:
Pulmonary hemorrhage and hemoptysis are the second-most common and potentially life-threatening complications after pneumothorax following percutaneous computed tomography-guided transthoracic lung biopsy (PCTLB). Preventing hemorrhagic complications after PCTLB requires an accurate estimation of risk factors. This study investigated the risk factors associated with pulmonary hemorrhage and hemoptysis following PCTLB, and whether the ratio of main pulmonary artery diameter (mPAD) to ascending aorta diameter (mPAD/AAD ratio) is a risk factor.
Methods:
We retrospectively analyzed 1,090 cases of PCTLB obtained from 1,050 patients using a core needle. The risk factors for overall pulmonary hemorrhage, higher-grade pulmonary hemorrhage, and hemoptysis were evaluated by multivariate analysis of patient characteristics, computed tomography (CT) imaging data including pulmonary artery diameter (mPAD) to ascending aorta diameter (mPAD/AAD) ratio, technical variables related to the biopsy, and pathologic findings.
Results:
Pulmonary hemorrhage occurred in 31.38% (342/1,090) of PCTLB cases, including lower-grade (24.4%, 266/1,090) and higher-grade hemorrhage (6.97%, 76/1,090). The incidence of hemoptysis was 3.03% (33/1,090). Multivariate analysis revealed significant associations between overall pulmonary hemorrhage and lesion location in the lower lobe, subsolid and smaller lesions, greater lesion depth, and lung metastases. For higher-grade pulmonary hemorrhage, an mPAD/AAD ratio >1, smaller lesions, greater lesion depth, emphysema, and lung metastases were risk factors. Risk factors for hemoptysis were history of hypertension and lower- and higher-grade pulmonary hemorrhage.
Conclusions:
Pulmonary artery enlargement detected by CT (mPAD/AAD ratio >1) is independently associated with higher-grade pulmonary hemorrhage following PCTLB.
Tumoral pulmonary hypertension (PH) comprises a variety of subtypes in patients with a current or previous malignancy. Tumoral PH principally includes the tumour-related pulmonary microvascular conditions pulmonary tumour microembolism and pulmonary tumour thrombotic microangiopathy. These inter-related conditions are frequently found in post mortem specimens but are notoriously difficult to diagnose ante mortem The outlook for patients remains extremely poor although there is some emerging evidence that pulmonary vasodilators and anti-inflammatory approaches may improve survival. Tumoral PH also includes pulmonary macroembolism and tumours that involve the proximal pulmonary vasculature, such as angiosarcoma; both may mimic pulmonary embolism and chronic thromboembolic PH. Finally, tumoral PH may develop in response to treatments of an underlying malignancy. There is increasing interest in pulmonary arterial hypertension induced by tyrosine kinase inhibitors, such as dasatanib. In addition, radiotherapy and chemotherapeutic agents such as mitomycin-C can cause pulmonary veno-occlusive disease. Tumoral PH should be considered in any patient presenting with unexplained PH, especially if it is poorly responsive to standard approaches or there is a history of malignancy. This article will describe subtypes of tumoral PH, their pathophysiology, investigation and management options in turn.
Since the 1st World Symposium on Pulmonary Hypertension (WSPH) in 1973, pulmonary hypertension (PH) has been arbitrarily defined as mean pulmonary arterial pressure (mPAP) ≥25 mmHg at rest, measured by right heart catheterisation. Recent data from normal subjects has shown that normal mPAP was 14.0±3.3 mmHg. Two standard deviations above this mean value would suggest mPAP >20 mmHg as above the upper limit of normal (above the 97.5th percentile). This definition is no longer arbitrary, but based on a scientific approach. However, this abnormal elevation of mPAP is not sufficient to define pulmonary vascular disease as it can be due to an increase in cardiac output or pulmonary arterial wedge pressure. Thus, this 6th WSPH Task Force proposes to include pulmonary vascular resistance ≥3 Wood Units in the definition of all forms of pre-capillary PH associated with mPAP >20 mmHg. Prospective trials are required to determine whether this PH population might benefit from specific management.
Regarding clinical classification, the main Task Force changes were the inclusion in group 1 of a subgroup “pulmonary arterial hypertension (PAH) long-term responders to calcium channel blockers”, due to the specific prognostic and management of these patients, and a subgroup “PAH with overt features of venous/capillaries (pulmonary veno-occlusive disease/pulmonary capillary haemangiomatosis) involvement”, due to evidence suggesting a continuum between arterial, capillary and vein involvement in PAH.
Background
There are many epidemiological pieces of evidence that show IPF patients have the highest risk of lung cancer. We conducted a systematic review of all published data to define the characteristics of lung cancer that develops in IPF by performing a meta-analysis.
Method
This study was performed based on the PRISMA guideline. Documents gathered by searching through the Web of Sciences, Scopus, PubMed/Medline, OVID, and COCHRANE databases which published before 03/25/2018 that related to lung cancer in IPFs’ patients. Articles were searched using standard keywords as well as Mesh and Mesh Entry and all probabilistic combinations of words using Boolean operators. Data searching, extracting and quality appraising were done by two researchers, independently. At last, Random-effects size based on Cochrane test and I² were used. The review protocol has been registered in PROSPERO with ID: CRD42018094037.
Results
Based on the meta-analysis conducted in 35 (0.18%) included studies, the total sample size of patients with IPF was estimated 131947 among whom 6384 had LC. The total rate of LC prevalence in IPF patients was estimated to be 13.54% (95% CI: 10.43–17.4) that was significantly 9 times higher in men vs. Women and smoker vs. non-smoker. Highest to lowest prevalence of cellular (histological) subtypes of lung cancer in IPF were SQCC (37.82%), ADC (30.79%), SmCC (20.48%), LCC (5.21%), and ADQC (4.81%), respectively. The highest and lowest stage of lung cancer in IPF patients was estimated at III and II, respectively. The highest involvement location of lung cancer in IPF patients was in the Peripheral. Also, the prevalence of the tumor region involved from the highest to the lowest was estimated to be in the RLL, LLL, RUL and LUL regions.
Conclusions
Lung cancer in IPF, most commonly SQCC, presents in elderly heavy smokers with a male, locating in peripheral regions and the lower part of lung predominance.
Background:
Pulmonary hypertension (PH) is a severe, progressive disease. Although 5 PH subgroups are recognized, reports on survival have focused mainly on pulmonary arterial hypertension (PAH).
Methods:
Long-term transplant-free survival and its determinants were investigated in patients with PH (diagnosed by right heart catheterization) within a prospective registry at a single referral center in Giessen, Germany.
Results:
In total, 2,067 patients were enrolled (PAH, 685 patients [33.1%]; pulmonary venous hypertension, 307 patients [14.9%]; PH due to lung diseases (LD-PH), 546 patients [26.4%; mainly interstitial lung disease and chronic obstructive pulmonary disease]; chronic thromboembolic PH, 459 patients [22.2%]; PH owing to miscellaneous/unknown causes, 70 patients [3.4%]). Median follow-up was 37 months. Differences in transplant-free survival between etiologic groups were highly significant (p < 0.001), with 1-, 3- and 5-year survival rates of 88.2%, 72.2% and 59.4%, respectively, for those with PAH compared with 79.5%, 52.7% and 38.1%, respectively, for patients with LD-PH. Patients' age, gender and 6-minute walk distance (6MWD), but not New York Heart Association (NYHA) functional class, associated significantly with survival across all PH subtypes in multivariate Cox regression analyses.
Conclusions:
This is the largest single-center PH cohort described so far. Some parameters used in clinical practice do not independently predict survival. Age, gender and 6MWD outperformed NYHA functional class in predicting survival across all etiologic groups.
Background and objective
Patients with pulmonary hypertension (PH) are considered to be at risk for complications associated with flexible bronchoscopy (FB), but data concerning the degree of PH are often lacking. We investigated whether COPD patients with PH who undergo bronchoscopy are at greater risk for complications.
Methods
This prospective study included 207 consecutive COPD patients undergoing FB. All underwent an echo-Doppler to evaluate pulmonary artery pressure on the day of the bronchoscopy procedure. Pulmonologists were blinded to the echocardiogram results.
Results
A total of 167 patients (80.7%) had normal pulmonary pressure. The remaining 40 patients (19.3%) had PH: 27 (13.0%) mild, eight (3.9%) moderate, and five (2.4%) severe. Noninvasive hemodynamic parameters between groups before and after FB were similar. Two patients with normal pulmonary pressure developed supraventricular tachycardia. None developed hemodynamically significant dysrhythmia. Bleeding episodes between groups in bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) did not differ. PH patients who underwent BAL and TBB had decreased O2 saturation during the procedure compared with the non-PH group (23.5% vs 6.9%, P=0.033). No deaths were attributable to FB.
Conclusion
PH is common among COPD patients undergoing FB. PH patients undergoing BAL and TBB are at higher risk of decreased O2 saturation than those without PH. Further studies should assess the risk among COPD patients with moderate-to-severe PH.
BACKGROUND: Animal studies and data from a single-center study suggest that tobacco smoke exposure may be a risk factor for precapillary pulmonary hypertension (PH).
OBJECTIVE: We aimed to survey tobacco smoke exposure in a large PH collective and to compare it with epidemiological data from healthy subjects.
METHODS: This is an international, multicenter, case-control study including patients with pulmonary arterial and chronic thromboembolic PH. All patients were asked specific questions about tobacco smoke exposure. Healthy controls were retrieved from the Swiss Health Survey (n = 18,747).
RESULTS: Overall (n = 472), 49% of PH patients were smokers and there was a clear sex difference (women 37%, men 71%). Significantly more PH men were smokers compared with healthy controls, whereas less PH women were ever active smokers. However, 50% of the non-smoking PH women were exposed to secondhand smoke, leading to a significantly higher number of tobacco smoke-exposed individuals compared to healthy controls. PH smokers were significantly younger compared to those not exposed.
CONCLUSION: Active and environmental tobacco smoke exposure is common in PH. The higher prevalence of male PH smokers, the higher exposure to environmental tobacco smoke in PH women compared to healthy controls and the lower age at PH diagnosis in smokers may indicate a pathogenic role of tobacco smoke exposure in PH.
Lung cancer is the main cause of cancer death in France. The diagnosis is often late and the delay between the onset of symptoms and management is considered an aggravating factor.
Our prospective study collected the dates of the start of management of 139 consecutive patients receiving first line treatment for thoracic cancer in our hospital between November 2008 and May 2009. The aim of this study was to evaluate the delays in medical or surgical treatments in patients with thoracic cancer and to determine the cause of these delays.
The median delay between the first abnormal chest X-ray and treatment was 9.6 weeks. The delays were significantly shorter in the late stages and in small cell cancer (P=0.001). There was a tendency for shorter delays in women and for longer delays in older patients.
Evaluation of the delays in treatment, particularly in the early stages, is part of the quality control of management of these diseases.
Pulmonary hypertension is associated with higher mortality rates. The associations of nondialysis-dependent CKD and all-cause mortality in patients with pulmonary hypertension were studied.
The study population included those patients who underwent right heart catheterization for confirmation of pulmonary hypertension between 1996 and January 2011. Pulmonary hypertension was defined as the presence of mean pulmonary artery pressure≥25 mmHg at rest measured by right heart catheterization. CKD was defined as the presence of two measurements of eGFR<60 ml/min per 1.73 m(2) 90 days apart. The risk factors associated with CKD as well as the association between CKD and death in those patients with pulmonary hypertension using logistic regression and Cox proportional hazard models were examined.
Of 1088 patients with pulmonary hypertension, 388 (36%) patients had CKD: 340 patients had stage 3 CKD, and 48 (4%) patients had stage 4 CKD. In the multivariable analysis, older age, higher hemoglobin, and higher mean right atrial pressures were independently associated with CKD. During a median follow-up of 3.2 years (interquartile range=1.5-5.6 years), 559 patients died. After adjusting for relevant covariates, presence of stage 3 CKD (hazard ratio, 1.37; 95% confidence interval, 1.14 to 1.66) and stage 4 CKD (hazard ratio, 2.69; 95% confidence interval, 1.88 to 3.86) was associated with all-cause mortality in those patients with pulmonary hypertension. When eGFR was examined as a continuous measure, a 5 ml/min per 1.73 m(2) lower eGFR was associated with a 5% (95% confidence interval, 1.03 to 1.07) higher hazard for death. This higher risk with CKD was similar irrespective of demographics, left ventricular function, and pulmonary capillary wedge pressure.
In a clinical population referred for right heart catheterization, presence of CKD was associated with higher all-cause mortality in those patients with pulmonary hypertension. Mechanisms that may underlie these associations warrant additional studies.
This article is intended to provide an overview of the anesthetic management for bronchoscopic procedures in patients with pulmonary hypertension (PH). This includes the classifications of PH, diagnosis with severity, and treatment modalities as detailed knowledge of this condition is imperative for proper anesthetic management. Preoperative evaluation and optimization of the patient is discussed as well. Bronchoscopic procedures require airway manipulation and compromise ventilation for lengths of time. As hypoxemia and hypercarbia trigger decompensation in PH, this may lead to a downward spiral if control is lost. Therefore a discussion of the intraoperative anesthetic management and the critical concerns are detailed in this article, as well as treatment modalities and management for said concerns.
Non–small cell lung cancer (NSCLC) is the leading cause of cancer-related death in the United States. With the implementation of lung cancer screening, the number and proportion of patients diagnosed with early-stage disease are anticipated to increase. Surgery is currently the standard of care for patients with operable stage I NSCLC. However, promising outcomes with stereotactic body radiation therapy (SBRT) in patients with inoperable disease has led to interest in directly comparing SBRT and surgery in operable patients. Unfortunately, early randomized trials comparing surgery and SBRT closed early because of poor accrual. In this article, the nuances of surgery and SBRT for early-stage NSCLC are reviewed. Furthermore, retrospective and prospective analyses of SBRT in early-stage NSCLC are discussed, and active randomized trials comparing these 2 approaches are described. Cancer 2017. © 2017 American Cancer Society.
Both COPD and emphysema are associated with an increased incidence of lung cancer, but the impacts of these comorbidities on lung cancer prognosis are still unclear. Herein, we conducted a meta-analysis to clarify whether the presence of these comorbidities indicates poor survival in patients with lung cancer. A comprehensive search was conducted using PubMed, Embase, Web of Science, ASCO Abstracts and Cochrane library for articles published before 1 June 2015. Papers referenced by the obtained articles were also reviewed. Main outcomes were overall survival (OS) and disease-free survival (DFS) in patients with lung cancer. Pooled hazard ratio (HR) and 95% confidence intervals (CIs) were calculated using random-effects models. Subgroup and sensitivity analyses were also conducted. Of 58 full texts reviewed, 26 met our inclusion criteria that were derived from 21 and seven studies examining the impacts of COPD and emphysema on survival of lung cancer, respectively. Meta-analyses revealed that concomitant COPD was associated with poorer OS (HR, 1.17; 95% CI: 1.10-1.25, n = 20), which was independent of tumour staging, diagnostic criteria of COPD or location, and DFS (HR, 1.52; 95% CI: 1.04-2.23, n = 6) with high heterogeneity (I(2) = 78%). The presence of emphysema in patients with lung cancer predicted worse OS (HR, 1.66; 95% CI: 1.25-2.22, n = 7), but not poorer DFS. The presence of COPD and emphysema are robust predictors of poor survival in patients with lung cancer. Early detection of these diseases should be taken into account for lung cancer surveillance and management.
Guidelines summarize and evaluate all available evidence on a particular issue at the time of the writing process, with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk-benefit ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate.
Pulmonary hypertension is considered a poor prognostic factor for or even a contraindication to major lung resection, but evidence for this claim is lacking. This study evaluates the impact of pulmonary hypertension on morbidity and mortality following pulmonary lobectomy.
Adult patients who underwent a lobectomy for cancer and had a transthoracic echocardiogram (TTE) performed within the year prior to the operation were included. Pulmonary hypertension was defined as an estimated right ventricular systolic pressure (RVSP) of ≥36 mmHg by TTE. The preoperative characteristics, intraoperative data and postoperative outcomes of patients with and those without pulmonary hypertension based on TTE were compared. A model for morbidity including published risk factors as well as pulmonary hypertension was developed by multivariable logistic regression.
There were 279 patients without pulmonary hypertension and 19 patients with pulmonary hypertension. Patients with pulmonary hypertension had a lower preoperative forced expiratory volume in 1 s and diffusing capacity of the lung for carbon monoxide than patients without pulmonary hypertension and a higher incidence of tricuspid regurgitation and mitral regurgitation, but the groups were otherwise similar. The mean RVSP in the group of patients with pulmonary hypertension was 47 mmHg. Perioperative mortality (0.0 vs 2.9%; P = 1.0) and postoperative complications (57.9 vs 47.7%; P = 0.48) were not significantly different between patients with and those without pulmonary hypertension. The presence of pulmonary hypertension was not a predictor of adverse outcomes in either univariate or multivariate analysis.
Lobectomy may be performed safely in selected patients with pulmonary hypertension, with complication rates comparable with those experienced by patients without pulmonary hypertension.
The association between systemic sclerosis (SSc) and cancer was widely described, particularly with breast and lung carcinoma; while, data regarding possible associations between cancer and SSc features are still scarce. We retrospectively evaluated the prevalence of lung cancer in our SSc patient cohort (318 SSc patients, 31 M and 287 F, age 51.5±14.5SD years, disease duration 10.3±6.5SD years) and clinico-serological factors potentially associated to the development of this malignancy. A review of the world literature about this topic was also done. We found that lung cancer complicated 16/318 (5%) SSc patients; namely 11/287 females (4%) and 5/31 males (16.1%). Median age of SSc patients with lung cancer was 54 (range 38-72) years for female patients, and 63 (range 40-73) for males; 13/16 patients died because of the neoplasia. Considering the incidence of lung carcinoma in sex/age-matched general population of the same geographical area, the percentages of lung cancer in our SSc series are about 2.5 and >5 times higher for male and female patients, respectively. The presence of lung cancer significantly correlated with male sex (p=0.011), presence of anti-Scl70 antibodies (p=0.0007), cyclophosphamide therapy (p=0.0001), forced vital capacity (FVC) <75% (p=0.0001), and lung fibrosis (p=0.0127); moreover patients with cancer have a significantly lower age at the diagnosis of SSc (p=0.009) and longer disease duration (p=0.0175). The logistic regression analysis confirmed a significant association with the anti-Scl70 antibodies (OR 6.4, 95%IC 1.7-24.1; p=0.006) and the reduction of FVC (OR 6.7, 95%IC 2.2-20.7; p=0.001) only. Overall, the prevalence of lung cancer in the subset of SSc patients with anti-Scl70 antibodies was 12/105 (11.4%), 9/40 (22.5%) in patients with FVC% reduction, and 7/22 (31.8%) in patients with both. In literature, the median prevalence of lung cancer in SSc series was 2.4% (range 0-4.2%); even if sporadic, associations with lung involvement or antiScl70 autoantibodies were raised, according to our findings. Our study confirmed the higher frequency of lung cancer among SSc patients compared to general population, particularly within patients' subset with serum anti-Scl70 antibodies and lung involvement.
Literature about thoracic surgery in patients with pulmonary hypertension is scarce. Perceived high risk has appropriately discouraged any unnecessary operation. However, the medical therapy for pulmonary hypertension has made great advances during the last decade. It is likely that future advances in survival and possibly the need for diagnostic procedures will increase the anesthesiologist's exposure to such patients. Understanding the unique physiology as well as new therapeutic agents will facilitate safe care for these challenging patients.
Since 1998, there have been three World Heath Organization symposiums on pulmonary hypertension. The most recent meeting in 2008 at Dana Point included revisions of the classification scheme and updates on new trials and therapies. New drugs have been utilized in cardiac, lung, or liver transplant operations to treat pulmonary hypertension. It is also recognized that one-lung ventilation presents unique problems for the patient with pulmonary hypertension. Inhalation use of the new pulmonary vasodilator drugs represents a new frontier for intraoperative pharmacology.
Here, the various types of pulmonary hypertension, physiologic changes, and new drug therapies are reviewed. Clinical experience with patients with pulmonary hypertension undergoing both nonthoracic and thoracic procedures is also reviewed. By identifying potential problem areas and application of new pharmacology, an approach to the patient with pulmonary hypertension is synthesized.
Pulmonary arterial hypertension (PAH) is an orphan disease for which the trend is for management in designated centers with multidisciplinary teams working in a shared-care approach.
To describe clinical and hemodynamic parameters and to provide estimates for the prevalence of patients diagnosed for PAH according to a standardized definition.
The registry was initiated in 17 university hospitals following at least five newly diagnosed patients per year. All consecutive adult (> or = 18 yr) patients seen between October 2002 and October 2003 were to be included.
A total of 674 patients (mean +/- SD age, 50 +/- 15 yr; range, 18-85 yr) were entered in the registry. Idiopathic, familial, anorexigen, connective tissue diseases, congenital heart diseases, portal hypertension, and HIV-associated PAH accounted for 39.2, 3.9, 9.5, 15.3, 11.3, 10.4, and 6.2% of the population, respectively. At diagnosis, 75% of patients were in New York Heart Association functional class III or IV. Six-minute walk test was 329 +/- 109 m. Mean pulmonary artery pressure, cardiac index, and pulmonary vascular resistance index were 55 +/- 15 mm Hg, 2.5 +/- 0.8 L/min/m(2), and 20.5 +/- 10.2 mm Hg/L/min/m(2), respectively. The low estimates of prevalence and incidence of PAH in France were 15.0 cases/million of adult inhabitants and 2.4 cases/million of adult inhabitants/yr. One-year survival was 88% in the incident cohort.
This contemporary registry highlights current practice and shows that PAH is detected late in the course of the disease, with a majority of patients displaying severe functional and hemodynamic compromise.
The specific incidence of thrombotic pulmonary embolism (PE), tumor PE and tumor invasion into large veins according to tumor type and tumor site remains unclear.
A total of 65,181 cancer patients were identified from 98,736 postmortem examinations. Thrombotic PE occurred in 2.32% of all cancer patients and comprised 88.6% of the total number of all PE events. The incidence of thrombotic PE was high in those with adenocarcinoma, leukemia and large cell carcinoma, and was low in those with hepatic cell carcinoma. The incidence of PE was high when tumor was present in hematogenous tissue, lungs, ovaries, pancreas and the biliary system, and was low when tumor was present in the liver. The incidence of tumor PE was high with large cell carcinoma, hepatic cell carcinoma and adenocarcinoma, and was also high when tumor was present in the lungs, ovaries, kidneys and liver. There was a significant correlation between the incidence of tumor PE and the incidence of tumor invasion into large veins.
The incidence of thrombotic PE, tumor PE and tumor invasion into large veins varies significantly according to tumor histopathology and tumor site.
Estimations Nationales de l'Incidence et de la Mortalité par Cancer en France Métropolitaine entre 1990 et 2018. Volume 1 : tumeurs Solides
- Defossez