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Biomedical subjects

K M Moser

Publications and source records attributed to K M Moser.

At least 73 records · Page 4Linked to original sources
PubMed1991

Catheter-based intravascular ultrasound imaging of chronic thromboembolic pulmonary disease.

Pulmonary thromboendarterectomy is now the treatment of choice for pulmonary hypertension due to chronic pulmonary thromboemboli. A precise assessment of location and extension of these thrombi is important because only proximal chronic pulmonary thromboemboli are accessible to surgery. Because intravascular ultrasound imaging can assess not only arterial luminal size, but also wall thickness, its value as a complement to angiography was assessed in 11 patients aged 35 to 64 years with severe pulmonary hypertension (systolic pulmonary artery pressure, mean +/- standard deviation 70 +/- 19 mm Hg; pulmonary artery resistance, 609 +/- 297 dynes.s.cm-5). Intravascular ultrasound was obtained in 10 of 11 patients and no complication occurred. Intravascular ultrasound identified 10 segments with suspected chronic pulmonary thromboemboli in 7 patients, all confirmed at operation. Nine segments were considered normal, all of which (except 1) were free of chronic pulmonary thromboemboli at operation. Image quality was highly dependent on pulmonary artery size and position of the catheter. Therefore, intravascular ultrasound of pulmonary arteries is feasible and safe in patients with pulmonary hypertension. It may help to assess the location and extension of the pathologic process involving pulmonary arteries.

Adult↗
PubMed1991

Epicardial activation and repolarization patterns in patients with right ventricular hypertrophy.

To map global epicardial repolarization patterns and test the "SI" model of T wave generation, the patterns of epicardial activation and repolarization in patients with chronic pulmonary thromboembolism and right ventricular hypertrophy were studied by computerized mapping techniques and monophasic action potential (MAP) recording. The ventricular activation patterns were characterized by delayed right ventricular activation and the absence of normal early epicardial ventricular breakthrough in some cases. The repolarization patterns were characterized by nonuniform distribution of T wave morphologies. The T waves were predominantly positive over the left ventricular epicardium and negative or biphasic over the right ventricular epicardium. The activation-recovery (A-R) intervals were measured from the local activation to the maximal dV/dt of the upstroke of the T waves (Wyatt method). The difference between the A-R intervals and the MAP from onset of activation to 90% repolarization (MAP90) varies according to T wave morphology and could be as high as 96 msec with positive T waves, despite significant correlations (r = 0.56-0.90) between MAP90 and A-R intervals for each morphology. Better overall correlations were found if the minimal dV/dt on the downslope of the positive T waves was chosen to estimate the time of local repolarization (alternative method). Using this method, the mean A-R intervals were the same over the right and left ventricles. Cardiopulmonary bypass significantly prolonged the action potential duration equally at all parts of the epicardium. We conclude that in patients with right ventricular hypertrophy, the time of local repolarization can be estimated by our alternative method; the right ventricle completes activation and repolarization later than the left ventricle, and the distribution of T wave morphologies is nonuniform, with predominantly positive T waves observed over the left ventricle and negative or biphasic T waves observed over the right ventricle. These findings are compatible with the SI model of the generation of T waves.

Action Potentials↗
PubMed1991

Chronic pulmonary thromboembolism in dogs treated with tranexamic acid.

BACKGROUND: Many questions remain regarding the pathogenesis, natural history, diagnosis, and treatment of chronic thromboembolic pulmonary hypertension in patients. To answer such questions, we developed an animal model of this disorder. The brisk thrombolytic response of canines to acute embolism has, previously, prevented the establishment of such a model. METHODS AND RESULTS: The fibrinolytic inhibitor tranexamic acid was given orally to canines before, and for intervals after, pulmonary emboli were released from venous thrombi formed in vivo in femoral veins or the inferior vena cava. Preliminary studies disclosed that embolic residuals from femoral vein thrombi were not sufficient to cause significant, persistent pulmonary hypertension. With repetitive, larger thrombi embolized from the inferior vena cava, however, persistent pulmonary hypertension was achieved in most animals. CONCLUSIONS: Resolution of emboli in the canine can be inhibited by tranexamic acid. As in humans, a spectrum of embolic residuals is encountered, and the perfusion lung scan consistently underestimates the extent of embolic residuals. Studies of this animal model continue.

Animals↗
PubMed1990

Current early results of pulmonary thromboendarterectomy for chronic pulmonary embolism.

Some patients with chronic pulmonary embolism causing severely symptomatic pulmonary hypertension have been managed by heart-lung transplantation with an associated hospital mortality of 24%. To allow comparison with pulmonary thromboendarterectomy (PTE), we have reviewed the hospital morbidity and mortality in 149 consecutive patients. From 1 October 1984 to 18 September 1989, these patients underwent PTE utilizing a standardized procedure consisting of median sternotomy, cardiopulmonary bypass, deep hypothermia and circulatory arrest for bilateral PTE in 91% (136/149) of the procedures with 7.4% (11/149) and 1.3% (2/149) undergoing right or left PTE, respectively. Ventilator dependency (greater than or equal to 5 days on respirator) occurred in 28.3% (41/146). Hospital mortality (death within 30 days or in hospital) was 11.4% (17/149). The most common causes of death were respiratory and multiorgan failure, 10 (59% of deaths) and acute pulmonary hemorrhage, 3 (17% of deaths). We conclude that PTE with an operative mortality of half that of heart-lung transplantation (11.4% vs. 24%) should be the procedure of choice for significantly symptomatic chronic pulmonary embolism. Furthermore, the hazards of immunosuppression and chronic graft rejection are avoided.

Adult↗
PubMed1990

Gas exchange in chronic thromboembolism after pulmonary thromboendarterectomy.

Thromboendarterectomy is the treatment of choice for chronic large vessel thromboembolic pulmonary hypertension. To identify the mechanisms responsible for the improvement in gas exchange following thromboendarterectomy, we studied nine patients with chronic thromboembolic pulmonary hypertension before and eight to 18 months after surgery using the multiple inert gas elimination technique. Preoperatively, all subjects had pulmonary hypertension and were hypoxemic or had an elevated P(A-a)O2. The VA/Q distribution was widened with an elevated VD/VT and a low cardiac index. After thromboendarterectomy, significant improvement had occurred. The VA/Q distribution had narrowed to near normal, and the cardiac index increased. It was concluded that thromboendarterectomy improved gas exchange both by improving VA/Q relationships and by increasing cardiac output.

Adult↗
PubMed1990

Pulmonary vascular steal in chronic thromboembolic pulmonary hypertension.

After pulmonary thromboendarterectomy, performed for relief of chronic thromboembolic pulmonary hypertension, perfusion lung scans have frequently disclosed new perfusion defects in segments served by undissected pulmonary arteries. Our hypotheses were that these new postoperative defects occurred with great frequency and did not represent postoperative vessel occlusion. We retrospectively reviewed the preoperative and postoperative perfusion scans of 33 consecutive patients undergoing pulmonary thromboendarterectomy. New postoperative perfusion defects were noted in 23 of 33 patients. The incidence of new defects was increased tenfold in segments that had (1) normal preoperative angiographic findings, (2) normal preoperative radionuclide perfusion, and (3) not been entered at the time of surgery. Postoperative angiograms, available in 15 of 33 patients, documented the nonembolic, nonocclusive nature of the new perfusion scan defects. The most plausible alternate explanation for this previously undescribed finding is a redistribution of pulmonary arterial resistance induced by the thromboendarterectomy, namely, a pulmonary vascular "steal."

Adult↗
PubMed1990

Risk factors for pulmonary thromboendarterectomy.

Pulmonary thromboendarterectomy is being performed with increasing frequency for incapacitating pulmonary hypertension caused by chronic large-vessel pulmonary embolism. However, patient-related risk factors and procedural complications associated with morbidity and mortality have not been fully defined. From Oct. 1, 1984, to April 10, 1989, we performed pulmonary thromboendarterectomy using deep hypothermia and circulatory arrest in 127 consecutive patients (62.2% male, mean age 50 +/- 16 [standard deviation], range 20 to 82 years) in whom the exposure and dissection of the pulmonary arteries and methods for myocardial protection have been standardized. End points for univariate and multivariate analyses of risk factors were reperfusion pulmonary edema leading to respiratory insufficiency as defined by ventilator dependency (greater than or equal to 5 days) (31.5%, 39/124) and hospital mortality (12.6%, 16/127). Multivariate analyses showed that ascites and need for 4 units of blood or more predicted ventilator dependency (p less than 0.03). Increased cardiopulmonary bypass times predicted both end points (p less than 0.03 to less than 0.0001), and failure to achieve at least a 50% reduction in pulmonary vascular resistance strongly predicted hospital death (p less than 0.0001). However, other factors that exhibited trends for association with one of the end points may prove important with a larger sample size. A hospital mortality rate of 12.6% for pulmonary thromboendarterectomy is acceptable when compared with approximately 25% for heart-lung transplantation, which is the only therapeutic alternative. Increased ventilator dependency and hospital mortality can be anticipated with longer cardiopulmonary bypass times and inadequate reduction of pulmonary vascular resistance.

Adult↗
PubMed1989

Mechanisms of hypoxemia in chronic thromboembolic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension is characterized by widespread central obstruction of the pulmonary arteries with organized thrombus and thereby differs substantially from other forms of pulmonary hypertension. We studied 25 patients using the multiple inert gas elimination technique to identify and quantitate the physiologic mechanisms of hypoxemia in this disorder. All patients had chronic obstruction of the central pulmonary arteries, which was demonstrated angiographically and later surgically confirmed. All patients but one were hypoxemic (PaO2 = 65 +/- 11 mm Hg, PaCO2 = 32 +/- 4 mm Hg, AaPO2 = 45 +/- 14 mm Hg), and all patients had pulmonary hypertension (mean Ppa = 45 +/- 11 mm Hg) with an elevated pulmonary vascular resistance (mean PVR = 1,000 +/- 791 dyne/s/cm5, normal less than 300). The cardiac index was reduced (1.7 +/- 0.6 L/min/m2), as was the P-vO2 (31 +/- 5 mm Hg). Inert gas studies revealed widened unimodal Va/Q distributions in 20 of 25 subjects, with a log standard deviation of 1.01 +/- 0.32 (upper limit of normal, 0.6; ages 20 to 40), shunt = 0.03 +/- 0.05 of cardiac output, and dead space of 3.4 +/- 1.1 ml/kg (upper limit of normal, 2.9). The VD/VT ratio was 0.51 +/- 0.10. No low (VA/Q less than 0.1) or high (VA/Q greater than 10.0) regions were present, and no evidence for diffusion limitation of O2 transfer at rest was found. The low cardiac output and resulting low P-VO2 were responsible for approximately 33% of the increased AaPO2. The magnitude of the VA/Q abnormality correlated poorly with the PVR, the mean Ppa, or the magnitude of vascular obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Analysis↗
PubMed1989

Patterns of pulmonary perfusion scans in normal subjects. IV. The prevalence of abnormal scans in smokers 30 to 49 years of age.

The usefulness of ventilation-perfusion scans in the diagnosis of pulmonary embolism is limited by the wide range of pulmonary diseases that are associated with abnormal scans, and by the largely undetermined prevalence of abnormal scans in persons without cardiopulmonary disease. In prior studies, we found perfusion defects to be rarely present in young persons and in older nonsmokers. To determine if normal older smokers have a higher prevalence of abnormal ventilation and perfusion scans, we performed six-view 99mTc perfusion (Q) scans and 133Xe ventilation (V) scans in 40 subjects 30 to 49 yr of age who had no known cardiopulmonary disease. Each subject had undergone a history, physical examination, electrocardiogram, spirometry, and posteroanterior chest roentgenogram prior to scanning. All V and Q scans were interpreted blindly and independently by two experienced readers. No subject demonstrated a lobar or segmental defect on two views. One subject had a matched subsegmental defect, and one subject had delayed washout from a subsegmental area of the right upper lobe during V scanning, with a normal Q scan. We conclude that abnormal V and Q scans are uncommon among normal smokers 30 to 49 yr of age.

Adult↗
PubMed1989

Chronic thromboembolic occlusion in the adult can mimic pulmonary artery agenesis.

In the first 100 patients operated on for C T-E PH, three were referred with the diagnosis of UPAA having been made elsewhere. We found that many features of these two conditions are so similar that differential diagnosis is very difficult. Shared features may include findings on chest x-ray film, pulmonary angiography, CT scan and MRI studies. Since the two conditions vary substantially with respect to the methods of potential surgical correction, recognition of this possible differential diagnostic dilemma is important.

Adult↗
PubMed1989

Management for interstitial lung disease. State of the art.

A survey of 109 pulmonary physicians representing both private practice and academic medicine was conducted to learn their practice of management and treatment of interstitial lung disease. Of the 109, 25 (23 percent) responded. Twenty-two of 23 routinely obtain tissue diagnosis. The routine method was transbronchial biopsy by 15 physicians vs open lung biopsy by seven. Few (n = 5) use BAL cell analysis. The majority of clinicians used two to four criteria to initiate therapy. Physiology laboratory data were the predominant criteria used by the majority of physicians and also were most commonly used to monitor a patient's course over time. Prednisone was the drug of choice for therapy. Immunosuppressive therapy was not used until failure of steroid therapy was observed. There was little consistency in the diagnostic procedures applied, criteria for the decision to treat, the drugs used to treat, or methods for monitoring.

Azathioprine↗
PubMed1989

Endobronchial metastases due to colorectal carcinoma.

Metastatic disease from colorectal carcinoma to the tracheobronchial tree has previously been reported in only 15 cases. Various modalities of treatment have been attempted but have met with limited success. We describe an additional nine cases, as documented by fiberoptic bronchoscopy, treated by Nd-Yag laser therapy debulking. Improvement in bronchial patency was evidenced visually in each case, and relief of symptoms occurred in eight cases. Survival periods of up to 21 months occurred. This type of metastatic disease may be more common than previously reported and combination therapy to include Nd-Yag laser debulking offers a safe and effective alternative in the palliative management of pulmonary symptoms and increased survival in select patients.

Adenocarcinoma↗
PubMed1989

Is lung sequestration of indium-111-labeled granulocytes organ specific?

Transient sequestration of polymorphonuclear leukocytes (PMN) in the normal lungs of animals occurred immediately following intravenous injection of 111In-labeled PMN. We investigated the organ specificity of this process. Equal amounts of homologous PMN, derived from the intravascular space and labeled with [111In]oxine, were infused either intravenously (i.v.) or intraarterially (i.a.) into pairs of rats. Changes in radioactivity emitted from three regions--representing lung, liver and spleen, and lower body--were determined from images during the following hour. A nonspecific character was demonstrated by the transient sequestration of activity in the lower body following i.a. infusions. However, the rate of initial clearance of activity (first 30 min) from the lungs of i.v.-infused rats was relatively slower than from the lower body of i.a.-infused rats. This suggests the presence of a lung-specific as well, which may be important for localization of PMN-related events to the lung.

Animals↗
PubMed1988

Intravenous administration of alpha-1-proteinase inhibitor in patients of PiZ and PiM phenotype. Preliminary report.

Nine patients with moderate pulmonary emphysema, six of PiZ phenotype and three of PiM phenotype, have received a single intravenous infusion of alpha-1-proteinase inhibitor (human) (A1PI), in a dose of 60 mg/kg over a 30-minute period. They also received a tracer dose (300 microCi) of 131I-labeled A1PI. No active or passive immunization against hepatitis was given. No acute toxicity was observed. Compared with baseline data, significant elevations of serum A1PI (measured both antigenically and as anti-elastase activity) occurred, with a serum half-life approximating 110 hours. Bronchoalveolar lavage fluid, obtained 48 hours after infusion, reflected a significant increase in A1PI concentration versus baseline bronchoalveolar lavage fluid values. Serial gamma camera images of the lungs confirmed persistence of enhanced lung radioactivity for several days. Urinary desmosine excretion did not change following A1PI infusion. During the period of follow-up thus far, no patient has had chronic toxicity, results of liver function tests have been stable, and there has been no development of hepatitis B antigen or antibodies to hepatitis B surface or core antigens.

Adult↗