Title Index for Volume 52: 2021

Comparative effects of verapamil and nitroprusside on left ventricular function in patients with hypertension

Pulmonary artery occlusion pressure and central venous pressure have been considered to be reliable measures of left and right ventricular preload in patients requiring invasive hemodynamic monitoring. Studies in recent years have questioned the correlation between these estimates of ventricular filling pressures and ventricular end-diastolic volumes/cardiac performance variables in specific patient groups, but clinicians have continued to consider the relationship valid in the broader context. The objective of this study was to assess the relationship between pressure estimates of ventricular preload (pulmonary artery occlusion pressure, central venous pressure) and end-diastolic ventricular volumes/cardiac performance in healthy volunteers. Prospective, nonrandomized, nonblinded interventional study. Cardiac catheterization and echocardiography laboratories. Normal healthy volunteers (n = 12 group 1, n = 32 group 2). Pulmonary catheterization and radionuclide cineangiography (group 1) and volumetric echocardiography (group 2) during 3 L of normal saline infusion over 3 hrs. In group 1, the initial pulmonary artery occlusion pressure and central venous pressure did not correlate significantly with initial end-diastolic ventricular volume indexes or cardiac performance (cardiac index and stroke volume index). Changes in pulmonary artery occlusion pressure and central venous pressure following saline infusion also did not correlate with changes in end-diastolic ventricular volume indexes or cardiac performance. In contrast, initial end-diastolic ventricular volume indexes and changes in these ventricular volume indexes in response to 3 L of normal saline loading correlated well with initial stroke volume index and changes in stroke volume index, respectively. The relationship between left ventricular end-diastolic volume index and stroke volume index was confirmed in group 2 subjects using mathematically independent techniques to measure these variables. In addition, initial central venous pressure, right ventricular end-diastolic volume index, pulmonary artery occlusion pressure, and left ventricular end-diastolic volume index failed to correlate significantly with changes in cardiac performance in response to saline infusion in group 1 subjects. Normal healthy volunteers demonstrate a lack of correlation between initial central venous pressure/pulmonary artery occlusion pressure and both end-diastolic ventricular volume indexes and stroke volume index. Similar results are found with respect to changes in these variables following volume infusion. In contrast, initial end-diastolic ventricular volume indexes and changes in end-diastolic ventricular volume indexes in response to saline loading correlate strongly with initial and postsaline loading changes in cardiac performance as measured by stroke volume index. These data suggest that the lack of correlation of these variables in specific patient groups described in other studies represents a more universal phenomenon that includes normal subjects. Neither central venous pressure nor pulmonary artery occlusion pressure appears to be a useful predictor of ventricular preload with respect to optimizing cardiac performance.

Left Ventricular Remodeling, Systolic Function, and Diastolic Function in Young Adults With β-Thalassemia Intermedia: A Doppler Echocardiography Study

Commentary: More ado about nothing: Resect “versus” respect and left ventricular function after repair

A112 Aims: A prolonged QT-Dispersion is associated with an increased risk of cardiovascular mortality and can be observed in patients after a myocardial infarction. In patients with kidney failure, the incidence of a myocardial infarction is highly increased. Moreover, dialysis treatment also modulates QT dispersion. In this study, a possible relation between QT-dispersion and left ventricular volume and mass indices should be investigated. Methods: 40 hemodialysis patients (20 with and 20 without coronary heart disease) were investigated. Echocardiography as well as ECG were performed before and after hemodialysis. Results: In patients with CHD, QT-Dispersion increased from 65.45 + 16.2 (SD) ms to 84.90 + 22.25 (SD) ms (p<0.002). In patients without CHD, no significant change in QT dispersion was detected. Echocardiography examination revealed a significant change in LVED from 5.81 + 1.08 (SD) cm to 5.09 + 1.2 (SD) cm (p<0,036) as well as LVVOL (p<0,047) and LVM (p<0,007) in patients with CHD. Correlation analysis showed no significant relation between QT-Dispersion and left ventricular mass and volume indices. Conclusions: This study shows, that changes in QT-Dispersion in hemodialysis patients are independent from alterations in left ventricular mass- and volume indices. Alterations in QT dispersion, however, are associated with CHD.

To characterize cardiac preload responsiveness in pediatric patients with cardiovascular dysfunction and dilated cardiomyopathy using global end-diastolic volume index, stroke volume index, cardiac index, and extravascular lung water index. Prospective multicenter observational study. Medical/surgical PICUs of seven Spanish University Medical Centers. Seventy-five pediatric patients (42 male, 33 female), median age 36 months (range, 1-207 mo), were divided into three groups: normal cardiovascular status, cardiovascular dysfunction, and dilated cardiomyopathy. All patients received hemodynamic monitoring with PiCCO2 (Pulsion Medical System SE, Munich, Germany). We evaluated 598 transpulmonary thermodilution sets of measurements. In 40 patients, stroke volume index, cardiac index, and global end-diastolic volume index were measured before and after 66 fluid challenges and loadings to test fluid responsiveness at different preload levels. Global end-diastolic volume versus predicted body surface area exhibits a power-law relationship: Global end-diastolic volume = 488.8·predicted body surface area (r = 0.93). Four levels of cardiac preload were established from the resulting "normal" global end-diastolic volume index (= 488.8·predicted body surface area). Stroke volume index and cardiac index versus global end-diastolic volume index/normal global end-diastolic volume index built using a linear mixed model analysis emulated Frank-Starling curves: in cardiovascular dysfunction group, stroke volume index (geometric mean [95% CI]) was 27 mL/m (24-31 mL/m) at "≤ 0.67 times normal global end-diastolic volume index," 37 mL/m (35-40 mL/m) at "> 0.67 ≤ 1.33 times normal global end-diastolic volume index" (Δ stroke volume index = 35%; p < 0.0001; area under the receiver-operating characteristic curve = 75%), 45 mL/ m (41-49 mL/m) at "> 1.33 ≤ 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 21%; p < 0.0001; area under the receiver-operating characteristic curve = 73%), and 47 mL/m (43-51 mL/m) at "> 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 4%; p = 1; area under the receiver-operating characteristic curve = 54%). In dilated cardiomyopathy group, stroke volume index was 21 mL/m (17-26 mL/m) at "> 0.67 ≤ 1.33 times normal global end-diastolic volume index," 27 mL/m (21-34 mL/ m) at "> 1.33 ≤ 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = 29%; p = 0.005; area under the receiver-operating characteristic curve = 64%), and 25 mL/m (20-32 mL/m) at "> 1.51 times normal global end-diastolic volume index" (Δ stroke volume index = -8%; p = 1; area under the receiver-operating characteristic curve = 54%). This study provides "normal" values for global end-diastolic volume index and limits of cardiac preload responsiveness in pediatric patients with cardiovascular dysfunction and dilated cardiomyopathy: 1.33 times normal global end-diastolic volume index represents the upper limit of patent cardiac preload responsiveness, with the highest expected responsiveness being below 0.67 times normal global end-diastolic volume index. The maximum response of the Frank-Starling relationship and therefore the level of no additional preload reserve is 1.33 to 1.51 times normal global end-diastolic volume index. Above 1.51 times normal global end-diastolic volume index preload responsiveness is unlikely, and the risk of pulmonary edema is maximal.

ABSTRACT: In humans, left atrial enlargement and reduced contractile functions are associated with adverse cardiovascular events and a poor prognosis in many dilatation of the left atrium occurs with the gradual evolution of chronic mitral valve disease and is well diseases. The left atrium is the most compromised cardiac chamber in dogs with chronic mitral valve disease (CMVD). Therefore, this study aimed to compare the main parameters of left atrial enlargement (left atrium/aorta ratio, left atrial diameter and volume indices) and contractile function (transmitral flow peak velocity A wave and time velocity integral, atrial fraction, and atrial ejection force) at different stages of valve disease, and correlate the left atrial diameter, volume, and contractile function indices with echocardiographic variables predictive of heart failure in dogs (transmitral flow peak velocity E wave, E wave/IVRT ratio, E wave/E´wave ratio, and E wave/A wave ratio). The results showed that progressive characterized by the left atrium/aorta ratio and left atrium volume index. The left atrial diameter and volume indices and left atrium/aorta ratio correlated positively with the transmitral flow peak velocity E wave and E wave/IVRT ratio, which are important indices of diastolic function. The left atrial contractile function indices increased as CMVD evolved. Except for the atrial fraction, the left atrial contractile function indices correlated with the left ventricular filling pressure indices.

Tables for calculation of color index, volume index and saturation index based on recently determined standards

To characterize the hemodynamic factors that regulate stroke volume during upright exercise in normal man, 24 asymptomatic male volunteers were evaluated by simultaneous right heart catheterization, radionuclide angiography, and expired gas analysis during staged upright bicycle exercise to exhaustion. From rest to peak exercise, oxygen consumption increased from 0.33 to 2.55 liters/min (7.7-fold), cardiac index increased from 3.0 to 9.7 liters/min per m2 (3.2-fold), and arteriovenous oxygen difference increased from 5.8 to 14.1 vol% (2.5-fold). The increase in cardiac index resulted from an increase in heart rate from 73 to 167 beats/min (2.5-fold), and an increase in left ventricular stroke volume index from 41 to 58 ml/m2 (1.4-fold). During low levels of exercise, there was a linear increase in cardiac index due to an increase in both heart rate and stroke volume index; stroke volume index increased as a result of an increase in left ventricular filling pressure and end-diastolic volume index and, to a much smaller extent, a decrease in end-systolic volume index. During high levels of exercise, further increases in cardiac index resulted entirely from an increase in heart rate, since stroke volume index increased no further. Left ventricular end-diastolic volume index decreased despite a linear increase in pulmonary artery wedge pressure; stroke volume index was maintained by a further decrease in end-systolic volume index. The degree to which stroke volume index increased during exercise in individuals correlated with the change in end-diastolic volume index (r = 0.66) but not with the change in end-systolic volume index (r = 0.07). Thus, the mechanism by which left ventricular stroke volume increases during upright exercise in man is dependent upon the changing relationship between heart rate, left ventricular filling, and left ventricular contractility. At low levels of exertion, an increase in left ventricular filling pressure and end-diastolic volume are important determinants of the stroke volume response through the Starling mechanism. At high levels of exertion, the exercise tachycardia is accompanied by a decrease in end-diastolic volume despite a progressive increase in filling pressure, so that stroke volume must be maintained by a decrease in end-systolic volume.

Heart rate-right ventricular volume relation with myocardial revascularization

This study investigated whether a small volume of 7.2% hypertonic saline solution (HSS) could affect M-mode echocardiographic indices in dogs. HSS induced significant increase in heart rate, stroke volume and cardiac index, when the fluid infusion was completed (P<0.05). In the HSS group, the left ventricular end-diastolic volume index, as an index of preload, significantly increased (P<0.05), whereas left ventricular end-systolic volume index were not altered. HSS induced slight increases in ejection fraction at end of infusion despite significantly differences were not observed. In conclusion, HSS did not induce a demonstrable effect on M-mode echocardiographic indices of systolic function-enhance cardiac contractility, but it caused preload augmentation that may contribute to an abrupt and transient increase in cardiac output just after HSS infusion.

Echocardiographic evaluation of cardiac remodelling in a cohort of patients with heart failure and reduced ejection fraction treated with dapagliflozin

Article1 May 1932Causes, Classification and Differential Diagnosis of AnemiasBased on the Detailed Examination of Over Two Hundred Patients and a Study of the LiteratureEDWIN E. OSGOOD, M.D., F.A.C.P., HOWARD D. HASKINS, M.D.EDWIN E. OSGOOD, M.D., F.A.C.P.Search for more papers by this author, HOWARD D. HASKINS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-5-11-1367 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis is a presentation of the views formulated during a seven years' study of the clinical and laboratory phases of anemias and the literature pertaining thereto. Details of the subjects chosen, technic used, and results of the color, volume and saturation index studies are given elsewhere.1It has long been customary to divide anemias into two groups. Under the term primary anemia were included cases of pernicious anemia and, sometimes, chlorosis; and under the name secondary anemia, all others. These names were given as the cause was supposed to be unknown in primary anemias and known in secondary anemias. Since...References1 OSGOODHASKINSTROTMAN EEHDFE: The value of accurately determined color, volume and saturation indices in anemias, Jr. Lab. and Clin. Med. To be published. Google Scholar2 ROBSCHEIT-ROBBINS FS: The regeneration of hemoglobin and erythrocytes, Physiol. Rev., 1929, ix, 666-709. CrossrefGoogle Scholar3 BAAR H: Progressive postinfektiöse Erythrophthise, Folia haemat, 1927, xxxv, 111-115. Google Scholar4 SELLING L: Benzol as a leucotoxin. Studies on the degeneration and regeneration of the blood and haematopoietic organs, Johns Hopkins Hosp. Rep., 1916, xvii, 83-142. Google Scholar5 MARTLAND HS: Occupational poisoning in manufacture of luminous watch dials; general review of hazard caused by ingestion of luminous paint, with especial reference to the New Jersey cases, Jr. Am. Med. Assoc., 1929, xcii, 466, 552-559. CrossrefGoogle Scholar6 ORDWAYGORHAM TLW: Diagnosis and treatment of diseases of the blood, Oxford Monographs, 1929, ix, Oxford University Press, New York. Google Scholar7 OSGOOD EE: Hemoglobin, color index, saturation index, and volume index standards; redeterminations based on the findings in one hundred and thirty-seven healthy young men, Arch. Int. Med., 1926, xxxvii, 685-706. CrossrefGoogle Scholar8 OSGOODHASKINS EEHD: Relation between cell count, cell volume, and hemoglobin content of venous blood of normal young women; redeterminations of color index, volume index, and saturation index standards based on observations in one hundred cases, Arch. Int. Med., 1927, xxxix, 643-655. CrossrefGoogle Scholar9 AUB JC: Lead poisoning, Med., 1925, iv, 1-250. Google Scholar10 HARTMANBROWNELL FAKA: The hormone of the adrenal cortex, Science, 1930, lxxii, 76. CrossrefGoogle Scholar11 MINOTMURPHY GRWP: Treatment of pernicious anemia by a special diet, Jr. Am. Med. Assoc., 1926, lxxxvii, 470-476. CrossrefGoogle Scholar12 JONESPHILLIPSLARSELLNOKES NWBIOHT: The hemopoietic effect of nuclear extractives in human anemias, Ann. Int. Med., 1929, ii, 603-621. Google Scholar13 STURGISISAACS CCR: Desiccated stomach in the treatment of pernicious anemia, Jr. Am. Med. Assoc., 1929, xciii, 747-749. CrossrefGoogle Scholar14 OSGOODWILHELM EEMM: Reticulocytes. Proc. Soc. Exper. Biol. and Med., 1931, xxix, 53-54. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Portland, Oregon*From the Departments of Medicine and Biochemistry, University of Oregon Medical School, Portland, Oregon.†Received for publication, July 30, 1931.Acknowledgment is due to P. Blakiston's Son & Co., Inc., 1012 Walnut St., Philadelphia, for permission to include in this article excerpts from the Textbook of Laboratory Diagnosis by Edwin E. Osgood and Howard D. Haskins. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDie Erkrankungen des erythrocytären Systems 1 May 1932Volume 5, Issue 11Page: 1367-1376KeywordsAnemiaBiochemistryClinical laboratoriesPernicious anemiaResearch laboratories Issue Published: 1 May 1932 PDF downloadLoading ...

Background: The role of epicardial adipose tissue (EAT) in heart failure with preserved ejection fraction (HFpEF) remains to be defined. Methods: A consecutive series of outpatients with chronic heart failure-heart failure with reduced ejection fraction (HFrEF) and HFpEF and/or diastolic dysfunction-had EAT assessed by echocardiographic measurement and related to indices of cardiac structure and function. Results: Epicardial fat thickness was significantly (p < 0.05) greater in HFpEF (N = 141) with a mean of 6.7 ± 1.6 mm compared with a mean of 5.1 ± 1.0 mm in HFrEF (n = 40). After adjusting for the relationship with BMI, in HFpEF, epicardial fat was significantly (p < 0.05) negatively correlated with left ventricular internal diameter end diastole (LVIDd), left ventricular internal diameter end systole (LVIDs), left ventricular (LV) end-diastolic volume (EDV) index, lateral e', septal e', right atrial (RA) volume index, and hemoglobin (Hgb). The association with Hgb was no longer significant after adjusting for the effect of age. HFpEF was associated with smaller LVIDd, LVIDs, LV EDV indexes, and left atrial (LA) and RA volume indexes. Conclusions: Epicardial fat is significantly (p < 0.05) greater in HFpEF than HFrEF. Epicardial fat is associated with smaller cardiac chamber sizes in HFpEF suggesting that epicardial fat acts as a constraint to cardiac dilation.

The aim of this study was to investigate to what extent mitotic activity index assessments are influenced by tumour heterogeneity. Ten invasive breast carcinomas of varying size were completely embedded, yielding 2-7 paraffin blocks per tumour. From each block, three H&E stained skip sections were cut and, in all sections, the mitotic activity index (MAI) and the mitoses per volume (M/V-)index were assessed. Coefficients of variation were calculated for the three different sampling levels (tumours, blocks, sections). In addition we recorded in how many tumours threshold discrepancies (values on both sides of the prognostic thresholds) occurred. Nested analysis of variance showed that most of the total variance occurred between the tumours. Threshold discrepancies occurred in four (40%) and five tumours (50%) for mitotic activity index and the mitoses per volume index, respectively. However, when grouping all sections from the same tumour and subjectively selecting the one showing the highest proliferation, the section with the highest mitotic activity was selected in nine of the 10 cases. In the other single case a prognostically correct value was still obtained. Thus, there is a noteworthy intra-tumour heterogeneity in mitotic activity in invasive breast cancer. We therefore propose the need to take multiple blocks per tumour and carefully scan all sections for the highest proliferative area.