Absence Of Pulmonary Congestion Research Articles

Evaluation of the effectiveness of two neural networks (Resnet50v2 and Inception V3) in identifying left atrial enlargement in adult dogs.

Mitral valve endocardiosis is a heart disease that is present in approximately 75% of cases of canine heart disease. Currently, the gold standard for diagnosis is echocardiography, but radiography provides us with valuable information for clinical staging of the disease, such as detecting left atrial enlargement, the presence or absence of pulmonary congestion and cardiogenic pulmonary edema more quickly. The aim of this study was to evaluate the effectiveness of two neural networks, Resnet50v2 and Inception V3, in detecting left atrial enlargement. A database was built with 1052 lateral images. The images were then separated into three distinct groups: 198 images with left atrial enlargement (LAA), 124 images with left atrial enlargement simultaneously with pulmonary edema (LAA_EP), totaling 322 images with left atrial enlargement and 580 images considered normal (N). As a result, all the models were > 90% accurate; Resnet50V2: 94.77%; Inception V3: 92.84%. In conclusion, the use of artificial neural networks to classify left atrial enlargement in radiographs of dogs is a viable approach that can help veterinary radiologists screen patients for left atrial enlargement.

2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

Early Diagnosis and Estimation of Pulmonary Congestion and Edema in Patients With Left-Sided Heart Diseases From Histogram of Pulmonary CT Number

To establish an early diagnosis and have a quantitative estimation of congestion or edema, pulmonary CT scans were performed to detect the increase of regional lung water volume of patients with congestive heart failure. CT scanning of the upper, middle, and lower lung fields at maximum inspiration and hemodynamic analysis to ensure a hemodynamically chronic stable condition after the heart failure therapy for 5 weeks by cardiac catheterization within 2 weeks before CT scanning were performed in 10 normal subjects and 25 patients with left-sided heart failure. Patients were divided into two groups according to the presence or absence of pulmonary congestion or edema on chest radiographs, and the mean pulmonary wedge pressure (mPWP). The pulmonary congestion group (14 patients) had pulmonary congestion or edema, and mPWP was greater than 13 mm Hg despite the heart failure therapy. The nonpulmonary congestion group (11 patients) had no pulmonary congestion or edema, and mPWP was lower than 10 mm Hg. Histograms of pulmonary CT numbers were graphed to a set region of interest (ROI) on transverse CT images in all subjects; then changes of pulmonary CT numbers when pulmonary congestion or edema occurred were estimated from those histograms. We found that when severe pulmonary congestion or edema occurred in 6 patients with severe left heart failure, the pulmonary CT numbers within the ROI rapidly increased from -650 to -750 Hounsfield units (HU). We defined the amount ratio between the pixels (pixel counts between -650 and -750 HU within these R0Is) and the pixels (pixel counts between -300 and -950 HU) of the CT number (which were all pixels composing these R0Is) x100(%) as "%PXL." %PXL showed a linear correlation with mPWP. Compared with the %PXL in the normal group, the %PXL in the pulmonary congestion group was significantly higher than that in the normal group (p<0.05, p<0.01, p<0.001) in all lung fields. Similarly, compared with the %PXL in the normal group, %PXL in the nonpulmonary congestion group was significantly higher than that in the normal group in the middle and lower lung fields (p<0.05, p<0.01) in the posterior field. From these results, we concluded that %PXL was a good index to identify abnormal water content usually not recognizable by routine chest radiograph in the lungs.

Effects of A Total Artificial Heart Right Stroke Volume Limiter on Left-Right Hemodynamic Balance

In a completely implantable total artificial heart (TAH), the left-right flow difference attributable to higher volumetric efficiency of the right pump and bronchial artery shunting has always been a significant problem. The automatic control of the Cleveland Clinic-Nimbus TAH accommodates for the left-right flow difference when the beat rate is below maximum (AUTO range). However, at its maximum beat rate (MAX), high left atrial pressure (LAP) (greater than 25 mmHg) with relatively low right atrial pressure (RAP) (less than 8 mmHg) were observed both in vitro and in vivo, suggesting the need for a stroke volume limiter (SVL) of the right pump. In vitro volume loading tests showed 10%, 15%, and 20% SVLs prevented a disproportionate increase of LAP. In vivo studies in five Holstein calves also showed a balanced LAP-RAP relationship with 10% and 15% SVLs at MAX. The left pump flow was not affected by this range of SVLs either in vitro or in vivo. Pulmonary function was maintained with either size SVL, with autopsies revealing absence of pulmonary congestion and minimal pleural effusions in two calves surviving for more than 1 month. Although additional studies are needed to determine the appropriate size of the SVL, both 10% and 15% SVLs were effective in maintaining left-right hemodynamic balance in this TAH.

Clinical evaluation of left ventricular diastolic performance

Diastole can be divided into four phases: isovolumic relaxation, early filling, diastasis, and atrial systole. The amount of LV filling that occurs during each of these phases depends on myocardial relaxation, the passive characteristics of the LV, the characteristics of the left atrium, pulmonary veins, and mitral valve, and the heart rate. When diastolic function is normal, the net effect of these factors results in an LV filling sufficient to produce an adequate cardiac output, while mean pulmonary venous pressure is maintained below 12 mm Hg. In the absence of systolic dysfunction, abnormal diastolic performance is usually due to abnormal relaxation and/or changes in the passive LV characteristics. Invasive studies can quantitate the rate of myocardial relaxation and the LV diastolic pressure-volume relation. More recently, RNA and Doppler echocardiography have been used to noninvasively evaluate diastolic performance by determining the pattern of LV diastolic filling. At rest, most LV filling occurs early in diastole. Conditions that produce diastolic dysfunction, such as LV hypertrophy and ischemia, are associated with reduced early diastolic filling and an augmented importance of atrial systole. It is important to recognize that such patterns can occur in patients who do not have clinically apparent diastolic dysfunction and in normals. Furthermore, a normal pattern can occur in patients who have severe diastolic dysfunction. A reduced early diastolic filling, in the absence of pulmonary congestion, indicates the loss of diastolic reserve, since the left atrium is being used as a booster pump. This pattern of diastolic filling in a patient who has symptoms of pulmonary congestion may suggest diastolic dysfunction, even if the systolic LV performance is normal. Since diastolic filling of the LV results from a complex interplay of factors, it is unlikely that a single, easily interpreted index of LV diastolic performance will ever be developed. However, the recent development of a noninvasive evaluation of the pattern of LV diastolic filling by RNA or Doppler echocardiography is an important advance. When interpreted with an understanding of the determinants of LV filling and the patient's clinical status, these noninvasive tests can contribute to the rational assessment of LV diastolic performance.

Risk stratification in patients with first non-q wave infarction: Limited value of the early low level exercise test after uncomplicated infarcts

Risk stratification using clinical and historical variables plus early low level exercise testing was performed in 141 patients with a first non-Q wave myocardial infarction. The 111 patients who performed the exercise test had a 3.6% cardiac mortality rate in the first year compared with 13.3% in the 30 patients who could not exercise (p = 0.063), and a 1 year incidence rate of recurrent cardiac events (cardiac death or recurrent nonfatal myocardial infarction) of 10.8% compared with 23.3% (p = 0.127). Patients who developed ischemia (ST depression or angina) during the test had an increased incidence of cardiac events in the year after the infarction (odds ratio >3, p < 0.05).When patients were subgrouped by the presence or absence of pulmonary congestion, the discriminatory value of the exercise test was seen to reside primarily in the cohort with pulmonary congestion. For example, ST depression during exercise in this group identified patients with a 71 % incidence of cardiac events in the year after the infarction compared with 5.3% for those without ST depression (odds ratio 45, p = 0.002). In the patients without pulmonary congestion, the exercise test had no discriminatory value.It is concluded that early low level exercise testing has a limited role after an uncomplicated non-Q wave infarction, but is useful in patients with clinical markers of higher risk.

Hemodynamic spectrum of “dominant” right ventricular infarction in 19 patients

In 19 patients right ventricular infarction was diagnosed on the basis of electrocardiographic features of acute inferior infarction and clinical evidence of elevation of systemic venous pressure and an absence of pulmonary congestion. Right heart catheterization documented elevated right ventricular end-diastolic pressure (mean 15.5 mm Hg) and commensurate right atrial pressure (mean 14.9 mm Hg). In all patients the pulmonary capillary wedge pressure (mean 13.2 mm Hg) was exceeded or equaled by the right ventricular end-diastolic pressure, suggesting a disproportionate reduction in right ventricular compliance or contractile function, or both. Thirteen patients were hypotensive (systolic blood pressure less than 100 mm Hg on admission), including six patients with cardiogenic shock. Right ventricular infarction is an uncommon and potentially reversible cause of cardiogenic shock;yet, in the experimental model, isolated right ventricular damage is relatively well tolerated. To identify the factors associated with systemic hypotension, data from patients with and without compromised systemic hemodynamic function were compared. In hypotensive patients, the right ventricular end-diastolic pressure was significantly higher (16.8 versus 12.8 mm Hg;p < 0.01) and reflected more extensive right ventricular damage. A pulmonary wedge pressure of 15 mm Hg or more was noted only among the hypotensive patients, and their wedge pressure (mean 14.8 mm Hg) was significantly greater than that of normotensive patients (mean 9.7 mm Hg, p < 0.05). Therefore, in patients with right ventricular infarction, an additional impairment of left ventricular function due to associated infarction of the inferior left ventricle is a significant factor causing hypotension. The elevated wedge pressure may influence right ventricular output by affecting pulmonary arterial diastolic pressure and right ventricular afterload. Right ventricular peak systolic pressure as an index of right ventricular afterload was significantly higher in hypotensive than in normotensive patients (30.5 versus 23.8 mm Hg, p < 0.03), and there was a linear correlation between this pressure and the pulmonary capillary wedge pressure (r = 0.895, p < 0.001). There was one hospital death (mortality rate 5.3 percent). Clinical management generally consisted of administration of fluids and digitalis and implantation of a temporary pacemaker. This study emphasizes the relatively favorable prognosis of this condition and suggests that aggressive diagnosis and management are appropriate.

Pure right ventricular infarction

The case is reported of a patient with chronic emphysema and cor pulmonale who developed the signs of acute myocardial infarction which were initially interpreted as being localized in the postero-inferior wall of the left ventricle. The patient rapidly developed the features of massive right heart failure in the absence of pulmonary congestion, a condition thought to be due to pulmonary emboli. The autopsy, however, revealed a pure right ventricular infarct, which covered more than half of the pre-existent right ventricular myocardium, in the setting of marked right ventricular hypertrophy infraction. The case furthermore shows that the possibility of pure right ventricular infarction should be evaluated in all patients with puzzling right heart failure, in the course of what initially is thought to be an acute left ventricular infraction, is important since therapy with plasma volume expanders should be used with great caution in such patients

Right atrial myxoma. Report of a case and review of the literature

Right atrial myxomas are rare tumors, but should be suspected in patients, especially women 35 to 55 years old, who have a relatively short history of progressing right heart failure, cyanosis, weakness and, sometimes, pulmonary embolism, and no history of rheumatic disease. A presystolic murmur, which varies with respiration, and a dominant A wave in distended neck veins can be found. A low arterial blood pressure, an elevated venous pressure, and a tendency toward polycythemia support the diagnosis, as do signs of right atrial hypertrophy in the electrocardiogram and radiographic evidence of enlargement of the right atrium and reduced vasculature of the lungs. Catheterization of the right side of the heart will show an elevated right atrial pressure and a diastolic pressure gradient over the tricuspid valve, and the course of the catheter may indicate the presence of a tumor. However, angiocardiography is the most reliable means of obtaining an exact diagnosis. Absence of pulmonary congestion without orthopnea, with a clear picture of congestive failure, conclusively shows that the tumor is situated in the right heart. The main differential diagnoses are valvular tricuspid stenosis, constrictive pericarditis, and carcinoid tumor. Patients with right atrial myxomas are good candidates for open-heart surgery, using extracorporeal circulation or hypothermia, and a high percentage of them will be cured.

Clinical test for pulmonary congestion with use of the Valsalva maneuver.

A relatively frequent and often perplexing problem in clinical medicine is the determination of the presence or absence of pulmonary congestion in the patient with suspected heart disease. Equally confusing at times is the differentiation of the symptoms due to pulmonary congestion from those due to primary pulmonary disease, particularly in the elderly patient complaining of shortness of breath. At present, the clinically available laboratory aids to the solution of these problems are radiographic examination of the chest and the measurement of the circulation time and vital capacity. However, the many variables inherent in these tests limit their usefulness, and not infrequently they offer no diagnostic aid in the detection of lesser degrees of pulmonary congestion. In the course of a physiological study of the Valsalva maneuver, we found that this maneuver could be adapted as a simple and reliable bedside method for the detection of the presence or absence