Canine biventricular performance during acute progressive pulmonary microembolization: Regional myocardial perfusion and fatty acid uptake

The cardiac output during acute pulmonary artery hypertension (PAH) may be compromised by right ventricular (RV) outflow obstruction, myocardial ischemia, or adverse ventricular interactions. To study the relative contributions of these mechanisms to impaired biventricular function during PAH, we injected 75 to 105-μm glass beads into the pulmonary vasculature of 11 dogs and correlated the hemodynamic alterations with changes in biventricular function. Biventricular ejection fractions and interventricular septal motion were evaluated by gated blood pool angiocardiograms. Regional myocardial blood flow (n = 8 dogs) was measured with microspheres, and regional myocardial fatty acid metabolism during PAH (n = 8 dogs) was assessed by measuring the regional myocardial extraction of the radioiodinated fatty acid analog, 15-(p-iodophenyl)-3-methylpentadecanoic acid (3m-PIP/PDA). Following microembolization, the mean pulmonary artery pressure increased from 14 ± 1 to 48 ± 2 mm Hg (P < .001) and cardiac output decreased from 3.5 ± 0.3 to 2.6 ± 0.3 1 /min (P < .05). Right ventricular volume increased and RV ejection fraction decreased progressively. Abnormal septal motion during PAH occurred in 5 of 11 dogs and was associated with decreased LV diastolic compliance. Right ventricular myocardial blood flow remained increased during PAH while the regional extraction of 3m-PIP/PDA was uniform throughout the heart. These findings suggest that during moderate PAH the canine cardiac output is limited by RV outflow obstruction and decreased LV diastolic compliance rather than by ischemia.     

Compensatory responses of left atrial conduit flow to atrial fibrillation with acute myocardial infarction in a canine model.

The aim of this study was to examine the interaction of acute atrial fibrillation (Af) and acute myocardial infarction (AMI) on left atrial (LA) and left ventricular (LV) filling in atrioventricular (A-V) sequential paced, open chest, anesthetized dogs. Left atrial conduit function was determined from pulmonary venous flow (PVF) and detailed analysis of early diastolic flow with the use of micromanometers and transmitral Doppler echocardiography. We studied 8 dogs with regular ventricular rates to avoid the confounding effect of ventricular arrhythmia in Af. In the control stage, Af increased the diastolic PVF volume to the left atrium compared with that during regular A-V pacing (from 0.58 +/- 0.11 mL/beat to 0.70 +/- 0.13 mL/beat, P <.05), as a compensatory response to the impaired systolic PVF volume (from 0.56 +/- 0.12 mL/beat to 0.41 +/- 0.11 mL/beat, P <.05). As a result, cardiac output was maintained. However, in the AMI stage, Af decreased cardiac output (from 0.95 +/- 0.32 L/min to 0.80 +/- 0.23 L/min, P <.05 versus AMI with A-V pacing), and decreased diastolic PVF volume (from 0.46 +/- 0.13 mL/beat to 0.33 +/- 0.14 mL/beat, P <.05 versus AMI with A-V pacing). These changes were associated with a prolonged LV isovolumic pressure decay rate. Our study demonstrates that Af does not affect cardiac output in the setting of normal LV function at a controlled ventricular rate because enhanced LA conduit flow compensates for impaired LA reservoir function. In contrast, in the setting of AMI, the compensatory response to Af is attenuated because of abnormal LV relaxation, resulting in a decrease in cardiac output.     

Left ventricular diastolic relaxation and pressure-diameter relations during ischaemic left ventricular failure in the dog

Summary. The significance of severe ischaemic left ventricular (LV) failure on the LV isovolumic relaxation process and diastolic chamber stiffness has been investigated in nine open-chest pentobarbital-anaesthetized dogs. LV failure was induced by bolus injections of 50 μm microspheres into left coronary vascular bed until LV minor axis diameter had increased about 25% and end-diastolic pressure about 20 mmHg. Such ischaemic LV failure did not shift the relation between diastolic LV pressure and minor axis diameter compared with pressure-diameter curves obtained before induction of failure. Neither inotropic nor chronotropic stimulation evoked such shifts. Assuming exponential pressure decline, LV relaxation was significantly slower during failure, but proceeded in all experimental conditions at rates which indicated complete relaxation in late diastole. Analysis of the pressure decline during LV relaxation demonstrated that this process proceeded faster than assumed by an exponential function both before and during LV failure.     

Gram-negative bacteremia produces both severe systolic and diastolic cardiac dysfunction in a canine model that simulates human septic shock.

A canine sepsis model that simulates the human cardiovascular response to septic shock was produced in 10 conscious unsedated dogs by implanting an Escherichia coli-infected clot into the peritoneum, resulting in bacteremia. By employing serial, simultaneous measurements of radionuclide scan-determined left ventricular (LV) ejection fraction (EF) and thermodilution cardiac index (CI), the end-diastolic volume index (EDVI) was calculated (EDVI = stroke volume index divided by EF). By using three different methods of quantifying serial ventricular performance (EF, shifts in the Starling ventricular function curve using EDVI vs. stroke work index, and the ventricular function curve response to volume infusion), this study provides evidence (P less than 0.01) that septic shock produces a profound, but reversible, decrease in systolic ventricular performance. This decreased performance was not seen in controls and was associated with ventricular dilatation (P less than 0.01); the latter response was dependent on an adequate volume infusion. Further studies of EDVI and pulmonary capillary wedge pressure during diastole revealed a significant, though reversible, shift (P less than 0.001) in the diastolic volume/pressure (or compliance) relationship during septic shock.     

Alterations in the peripheral circulation in COPD patients

RATIONALE: Although various factors influence peripheral circulation in chronic obstructive pulmonary disease (COPD) patients, little is known about the vasomotor changes in these subjects. OBJECTIVES: The present study was designed to assess alterations in the brachial circulation of COPD patients. METHODS: Twenty-five COPD patients and 25 healthy subjects were studied. Brachial artery (BA) blood flow and indices of BA stiffness were investigated by two-dimensional ultrasonography and pulsed Doppler. Cardiac dimensions, left ventricular (LV) function and cardiac output were assessed by pulsed Doppler echocardiography. MAIN RESULTS: A significant increase in LV mass was observed in the COPD group despite normal arterial pressure. Total arterial compliance and BA compliance were significantly decreased in COPD patients in comparison with healthy subjects. Heart rate was increased in COPD patients and was inversely correlated with PaO(2) and forced expiratory volume in the first second (FEV(1)). A decrease in LV preload was expressed by a reduction in LV diastolic diameters and LV stroke volume. Patients with severe COPD have a lower BA surface area than patients with moderate COPD. FEV(1) and PaO(2) were significantly related to BA compliance. CONCLUSION: In COPD patients, significant alterations in the peripheral circulation were observed. Moreover, the magnitude of changes in the peripheral circulation was related to the severity of COPD.     

Left ventricular diastolic function in patients with bronchial asthma

The aim of the study was to evaluate the diastolic function of the left ventricle (LV) in patients with bronchial asthma (BA) in relation to the phase and severity of the disease. Seventy four patients with BA, including 16 with mild persistent BA, 39 with moderate BA, and 19 with severe BA were examined in different phases of the disease. Echocardiography and Doppler study of intracardiac blood flow were performed and external respiratory function was studied. Thirty six healthy persons matched by age, gender, body weight, and blood pressure values made up a control group. Most characteristics of LV diastolic relaxation were found to become much worse in BA, which is due to bronchial obstruction, hypoxemia, dilatation, hypertrophy, and altered diastolic filling of the right ventricle (RV). LV diastolic filling improved when an exacerbation of BA attenuated. Worsening BA severity was ascertained to lead to decreased early LV filling, which is associated with enhanced bronchial obstruction, progressive RV hypertrophy and dilation, concentrated LV remodeling. The most likely mechanism of impaired transmitral blood flow in progressive BA is the impaired LV and RV interaction and pulmonary hemodynamic rearrangement. The revealed LV diastolic dysfunction in patients with BA of various severity and in different phases of the disease were not found to depend on heart rate changes.     

A re-evaluation of the hemodynamic consequences of intermittent positive pressure ventilation

The hemodynamic effects of intermittent positive pressure ventilation (IPPV) have generally been considered straightforward, being dominated by the inspiratory reduction in systemic venous return. Paradoxically, there is considerable debate regarding the effects of PEEP. We have studied both right ventricular (RV) and left ventricular (LV) performance during a single IPPV respiratory cycle in dogs with intact circulatory systems or the right heart bypassed in open and closed chest conditions. We have found that the "reverse pulsus paradoxus" during inspiration reflects both transmission of the increased intrathoracic pressure to the thoracic aorta and an increase in LV stroke volume (SV). This inspiratory increase in LVSV has been found to be influenced by, but not dependent on: (a) respiratory variations in RVSV; (b) variations in functional residual capacity or tidal volume altering pulmonary venous return and the degree of physical compression of the heart by the lungs; (c) an inspiratory decrease in RV volume, increasing LV diastolic compliance and, thus, probably improving pulmonary venous return; (d) a decreased transmural aortic diastole pressure reflecting an effective decrease in LV afterload produced by both the general increase in intrathoracic pressure and the direct compression of the heart; and (e) variations in the pulmonary vascular volume as indicated by changes in the transmural LV end-diastolic pressure. An understanding of IPPV during a single respiratory cycle facilitates an appreciation of the steady state hemodynamic effects of IPPV with or without PEEP. Our results imply that measurements made only at end-expiration, ignoring inspiratory events, may have serious limitations. Furthermore, they suggest that IPPV with PEEP should be evaluated as a form of LV assist in LV failure.     

Abnormal pulmonary vascular tone in canine oleic acid lung injury

OBJECTIVE: To characterize the endothelium-dependent and endothelium-independent components of abnormal pulmonary vascular tone in canine oleic acid lung injury. DESIGN: Prospective, interventional study. SETTING: University laboratory. SUBJECTS: Twenty anesthetized mongrel dogs. INTERVENTIONS: Right heart catheterization was performed to measure pulmonary vascular resistance before and after induction of oleic acid lung injury in ten anesthetized and ventilated dogs. Pulmonary and internal mammary artery rings were sampled in these ten dogs with oleic acid injury and in ten anesthetized healthy control dogs. We also studied the responses to acetylcholine, to phenylephrine, and to hypoxia of the intact or endothelium-denuded rings mounted in organ baths. MEASUREMENTS AND MAIN RESULTS: Oleic acid lung injury was associated with an increase in pulmonary vascular resistance from 118 +/- 11 to 245 +/- 47 dyne.sec.cm-5.m-2 and a decrease in the Pao2/Fio2 ratio from 451 +/- 42 to 139 +/- 26 mm Hg (mean +/- se, p <.05 and p <.01, respectively). Acetylcholine-induced relaxation was decreased in the oleic acid pulmonary artery rings compared with the controls (85 +/- 3% vs. 99 +/- 6% of precontraction level, p <.05). Phenylephrine-induced contraction was decreased in denuded oleic acid pulmonary artery rings compared with the controls (81 +/- 8% vs. 102 +/- 10% of contraction to KCl 120 mM, p <.05). In vitro hypoxia induced a small endothelium-dependent contraction followed by an endothelium-independent relaxation. These responses were not different in oleic acid lung artery rings and in controls, except for a decrease in hypoxic contraction in the oleic acid pulmonary artery rings. In vitro hypoxic pulmonary vasoconstriction and relaxation were, respectively, directly (r =.48) and inversely (r = -.67) correlated with oleic acid-induced increase in pulmonary vascular resistance. There was no correlation between in vitro internal mammary artery reactivity and oleic acid-induced increase in pulmonary vascular resistance. CONCLUSIONS: Oleic acid-induced lung injury slightly impairs pulmonary arterial endothelium-dependent relaxation and endothelium-independent contraction. In vitro hypoxic pulmonary vasoreactivity is related to in vivo oleic acid-induced increase in pulmonary vascular resistance.     

Left ventricular diastolic dysfunction in end-stage dilated cardiomyopathy: simultaneous Doppler echocardiography and hemodynamic evaluation

Left ventricular diastolic dysfunction is an integral component of end-stage dilated cardiomyopathy. To better characterize this disorder we studied 15 patients undergoing catheterization during cardiac transplant screening evaluation. Pulsed-wave Doppler echocardiographic recordings of mitral inflow were obtained with simultaneous high-fidelity left ventricular and phase-corrected pulmonary capillary wedge pressures. Doppler-derived isovolumic relaxation times were within normal limits, despite a prolonged coefficient of relaxation (tau), and correlated with pulmonary capillary wedge--left ventricular crossover pressure. Peak velocity of early diastolic filling was similar to that reported in normal subjects and did not correlate with crossover pressure or tau. Early diastolic acceleration and deceleration times were shortened compared with reported normal values. Acceleration time correlated with mean negative dP/dt from mitral valve opening to left ventricular minimum pressure and with crossover pressure, and deceleration time correlated with mean dP/dt from left ventricular minimum pressure to the peak of the rapid filling wave. Late diastolic filling at atrial contraction was absent in 12 patients, all of whom had a significant early diastolic rapid filling wave and an elevated end-diastolic pressure. Despite an increase in pulmonary capillary wedge pressure during atrial contraction, the failing ventricles were unable to generate detectable forward transmitral flow. Poor cardiac pump function was shown by low left ventricular stroke volume, which correlated with the diastolic flow velocity integral. Thus, in end-stage cardiomyopathy, the transmitral flow velocity pattern is characterized by normal peak early filling velocity, low normal isovolumic relaxation time, shortened acceleration and deceleration times of early diastolic flow, decreased early flow velocity integral, and absent or decreased filling during atrial contraction. This pattern reflects interaction between elevated transmitral driving pressure and the compromised relaxation and compliance of a left ventricle functioning on an elevated pressure-volume curve.     

Pulmonary dysfunction during paraquat-induced lung injury: a model of acute alveolar injury

Acute lung injury produced by paraquat causes progressive pulmonary insufficiency. To define the pattern of this injury, the sequence of changes in respiratory mechanics and pulmonary gas exchange was studied in eight mongrel dogs which received repetitive doses of paraquat intraperitoneally. Four other dogs served as controls. All dogs were studied while supine during halothane anesthesia. After baseline measurements, saline (control) or paraquat was administered and the studies repeated at 2, 4, 7, and 9 days. Control dogs showed no significant changes. Dogs receiving paraquat had reduced lung volume, decreased lung compliance with a shift of the static deflation pressure-volume curve downward and to the right, and hypoxemia which could not be entirely accounted for by an increased right-to-left intrapulmonary shunt. This study demonstrated that repeated doses of paraquat given intraperitoneally produced a pattern of acute lung injury in the dog which permitted the study of respiratory mechanics and gas exchange during progressive stages of lung injury.     

The Mechanism of Adaptation of Left Atrial Stretch Receptors in Dogs with Chronic Congestive Heart Failure

Chronic congestive heart failure (CHF) was induced in dogs by the construction of an aorto-caval fistula below the level of the renal arteries. Aorto-caval fistula dogs showed signs of CHF which included ascites, hind limb edema, and pulmonary congestion. Ventricular catheterization indicated a significantly higher left ventricular end diastolic pressure and lower maximum velocity of left ventricular pressure development/left ventricular end diastolic pressure in CHF dogs when compared to sham-operated controls. Heart weight/body weight ratios were significantly higher in CHF dogs. Electrophysiological recordings from medullated left atrial type B receptors from the cervical vagus indicated a depressed sensitivity of these receptors in CHF dogs when compared to sham-operated control dogs. For any given change in left atrial pressure, the discharge of left atrial receptors was significantly reduced in CHF dogs compared with sham-operated controls. The mechanism for this depressed sensitivity was investigated. Sonomicrometry of the left atrial appendage indicated a decreased compliance of the left atrial appendage in the dogs with chronic CHF. In addition, microscope examination of the complex unencapsulated receptor endings taken from the left atrial endocardium indicated a marked alteration in receptor morphology. A loss of the end arborization was the most typical finding. It is concluded that chronic CHF brought about by an aorto-caval fistula results in a depressed left atrial stretch receptor response and that both decreased left atrial compliance and structural alterations in the receptor endings may account for this depressed sensitivity.     

Atrial natriuretic peptide levels in plasma and in cardiac tissues after chronic hypoxia in rats

1. Atrial natriuretic peptide (ANP) levels were measured in cardiac tissues and in plasma from adult rats exposed to chronic alveolar hypoxia for periods of 2 h, 24 h and 7 days. Levels were also measured in rats that were maintained in hypoxia for 7 days and then returned to air for 24 h. 2. Plasma ANP was not altered at 2 h but was significantly increased at both 24 h and at 7 days. Plasma ANP in animals exposed to hypoxia for 7 days was normal 24 h after returning to air breathing, despite the persistence of indices of pulmonary hypertension. 3. No significant right atrial hypertrophy was observed under these conditions of chronic hypoxia. A reduction in right atrial ANP content was found at 24 h and was accompanied by a decrease in the number of electrondense granules per right atrial muscle cell. After exposure to hypoxia for 7 days, right atrial ANP and granule number was not different from control, and no alteration was found in right atrial ANP level after removal from the hypoxic environment. 4. No significant right ventricular hypertrophy was produced by exposure to hypoxia for 2 or 24 h. In the former group ventricular ANP had decreased significantly compared with control. Right ventricular hypertrophy was found in both the hypoxic groups after exposure for 7 days, when selective increases in right ventricular ANP content were found. 5. These findings are consistent with the hypothesis that ANP release occurs on exposure to chronic hypoxia and is independent of the associated cardiac hypertrophy and pulmonary vascular remodelling. The findings may have relevance to the natriuresis and reported changes in the renin-angiotensin-aldosterone axis under hypoxic conditions.     

多普勒超声评价慢性二尖瓣返流左室舒张功能

用脉冲多普勒超声技术对１８例慢性二尖瓣返流（ＣＭＲ）患者和２１例正常人进行二尖瓣舒张期血流频谱定量研究。结果表明，ＣＭＲ出现的假性正常的二尖瓣血流频谱，掩盖了左室舒张功能减退，实际为左室松驰功能障碍及顺应性降低所致。ＣＭＲ组的Ｅ波压差（Ｅ－ＰＧ）、Ａ波压差（Ａ－ＰＧ）、等容舒张时间（ＩＶＲＴ）、Ｅ波减速时间（Ｅ－ＤＴ）及左室充盈时间．（ＬＶＦ）等与正常对照组比较有显著性差异（Ｐ＜０．０１），是ＣＭＲ情况下反映左室舒张功能减退的综合评价指标。     

Angiotensin converting enzyme activity in the clinical course and forming of cor pulmonale in patients with chronic obstructive pulmonary diseases

The aim of the study was to evaluate the influence of ACE in various biological media (blood, sputum, and lung tissue) on the clinical manifestations and morphofunctional cardiac variables in 137 patients with chronic obstructive pulmonary disease (COPD), of whom 17% had mild, 70% had medium, and 13% had severe degree of the disease according to Federal program, 1999. Seventy percent of the patients had stage II pulmonary hypertension according to Paleyev, 1986, while the number of patients with stage I and III was 14 and 16%, respectively. Circulatory insufficiency was mild (NYHA I to II) in 124 patients, and medium (NYHA III) in 13 patients only. The results of the study demonstrate that COPD exacerbation is accompanied by an increase in ACE activity, mostly in the lung tissue, induced sputum (IS), and, to a lesser degree, in blood serum; ISA CE activity is almost the same as that in the lung tissue. The study established a direct correlation between IS ACE activity and the level of C-reactive protein, an inflammatory process activity marker, and a reverse correlation between IS ACE activity and respiratory function variables, the latter characterizing bronchial obstruction. The study shows a strong direct correlation between IS ACE activity and the degree of right ventricular (RV) and left ventricular (LV) hypertrophy, as well as diastolic function disturbances according to RV isovolumetric relaxation time and LV early diastolic filling delay time. There is a strong reverse correlation between IS ACE activity and the disbalance of the ratio of blood flow velocities during early and late diastolic ventricular filling. The study found no significant correlations between ACE activity and the variables of ventricular systolic function. The study demonstrates a significant role of ACE activity changes in the progression of obstruction, inflammation, and myocardial remodeling.     

Ventricular interaction: from bench to bedside

Decreased right ventricle (RV) output results in decreased left ventricle end-diastolic volume (LVEDV) and output by series interaction. Direct ventricular interaction may also have a major effect on LV function. Thus, decreased LVEDV caused by reduced RV output may be further reduced by a leftward septal shift and pericardial constraint. This has been shown to be true in acute and chronic pulmonary hypertension and is now also apparent in severe congestive heart failure. The use of intracavitary LV end-diastolic pressure (LVEDP) to assess LVEDV is inappropriate if pressure surrounding the LV is increased: the surrounding pressure should be subtracted from LVEDP to calculate the effective distending (transmural) pressure which governs preload. If the surrounding pressure increases more than LVEDP, transmural LVEDP and LVEDV will decrease despite the increased LVEDP. Thus, the use of filling pressure to reflect changes in LVEDV has led to erroneous conclusions regarding changes in myocardial compliance and contractility. It is now clear that volume loading may reduce LVEDV and stroke work in pulmonary embolism, chronic lung disease and severe congestive heart failure despite increased LVEDP. The decreased stroke work is a result of reduced LV preload, not decreased contractility as would be suggested if filling pressure is used to reflect preload.     

Decreased and abnormal left ventricular filling in acute heart failure: role of pericardial constraint and its mechanism.

Pericardial constraining force is minimal in normal hearts; however, it is considered to be prominent in moderate to severe heart failure. Thus, effects of the pericardium on pulsed Doppler transmitral flow velocity pattern were examined in 17 dogs with acute left ventricular dysfunction. Left ventricular dysfunction with left ventricular end-diastolic pressure > or = 15 mm Hg was produced by injection of microspheres into the left coronary artery. Transmitral flow velocity pattern, left atrial and left ventricular diameters, and high-fidelity left atrial and left ventricular pressures were recorded before and after pericardiectomy. In five of the 17 dogs, mitral regurgitation with giant "v" wave of left atrial pressure occurred with reductions of left ventricular systolic pressure and peak rate of the left ventricular pressure fall (dP/dt) after pericardiectomy. In the other 12 dogs, peak early and late diastolic filling velocities increased with a decrease in left ventricular minimal pressure and increases in left arterial and left ventricular diameters and left atrial and left ventricular compliance after pericardiectomy. In these 12 dogs, left atrial to left ventricular crossover pressure, left ventricular end-diastolic pressure, and references for left ventricular relaxation did not change after pericardiectomy. Thus the release from pericardial constraining force in severe heart failure may increase chamber compliance of the left ventricle and left atrium and, in turn, increase peak early and late diastolic filling velocities through an increment in forward transmitral pressure gradient. Increased pericardial constraining force is a possible cause limiting left ventricular filling and hence cardiac output in heart failure.     

Role of Cytochrome P-450 in Alveolar Hypoxic Pulmonary Vasoconstriction in Dogs

Alveolar hypoxia induces pulmonary vasoconstriction by an unknown mechanism. Cytochrome P-450 (C-P450) is found in the lung and may modify pulmonary vascular tone via its sensitivity to changes in oxygen tension or by affecting metabolism of a chemical mediator. Metyrapone and carbon monoxide are both inhibitors of C-P450. We tested alveolar hypoxic pulmonary vasoconstriction (AHPV) in 20 dogs before, during, and after separate administration of each inhibitor. Anesthetized dogs were ventilated through a double lumen endotracheal tube allowing ventilation of one lung with N(2) or CO as a hypoxic challenge and ventilation of the other lung with O(2) to maintain adequate systemic oxygenation. Distribution of lung perfusion was determined with intravenous (133)Xenon and external chest detectors. Before infusion of metyrapone, mean perfusion to the test lung decreased 30% with alveolar hypoxic challenge, but decreased only 10% during metyrapone infusion and returned to a base-line mean decrease of 31% after completion of metyrapone infusion. Prostaglandin F(2) alpha and angiotensin II infusions produced equivalent increases in pulmonary vascular resistance before and during metyrapone infusion. Before CO, mean test lung perfusion decreased 31% with alveolar hypoxia but was reduced only 10% from control when unilateral end-tidal CO% was >75%. Washout of alveolar CO with unilateral N(2) ventilation restored AHPV, with perfusion decreasing 29% from control. Thus, both metyrapone and carbon monoxide can reversibly inhibit AHPV. C-P450 may, therefore, be involved in the transduction process of the vasoconstrictor response to alveolar hypoxia.     

Aortic stiffness is related to left ventricular diastolic function in patients with diabetes mellitus type 1: assessment with MRI and speckle tracking strain analysis

Diabetes mellitus type 1 (DM1) is associated with aortic stiffening and left ventricular (LV) diastolic dysfunction, however the relationship between aortic stiffness and LV diastolic dysfunction in DM1 patients is still largely unknown. The purpose of this study was to evaluate whether an increased aortic stiffness, expressed by increased aortic pulse wave velocity (PWV), is associated with subclinical LV diastolic dysfunction and decreased left atrial (LA) compliance as assessed with speckle tracking strain analysis in patients with DM1. Aortic PWV was assessed with cardiovascular magnetic resonance in 41 DM1 patients. Patients underwent echocardiography for assessment of conventional LV diastolic function indices and LV and LA longitudinal strain and strain rate (SR) assessed with speckle tracking strain analysis. LV SR during the isovolumic relaxation period (SRIVR) and LA strain were recorded and the E-wave velocity to SRIVR velocity ratio (E/SRIVR) was calculated. Independent samples t test and multivariate linear regression analyses were used for statistical analyses. Aortic PWV significantly correlated with SRIVR (β = ?0.71, p < 0.001), E/SRIVR (β = 0.61, p = 0.002) and LA strain (β = ?0.47, p = 0.014), but not with conventional echocardiographic markers of diastolic function (all p > 0.10). In DM1 patients, aortic stiffness is inversely associated with sensitive markers of LV diastolic function and decrease in LA compliance as measured with echocardiographic speckle tracking strain analysis.     

Pulmonary capillary pressures during hypoxia and hypoxemia: experimental and clinical studies

Unlike the systemic circulation, the pulmonary vasculature constricts in response to hypoxia to divert blood flow to better-ventilated segments. The site of this response, the hypoxic pulmonary vasoconstriction, has been reported as precapillary in numerous experimental models of isolated animal lungs. In the present study, the response of intact chest dog and human lungs to hypoxia and hypoxemia, respectively, was also precapillary vasoconstriction. In dogs, hypoxia in the ipsilateral lung attenuated the normal vertical blood flow gradient. Contralateral hypoxia did not alter pulmonary regional blood flow, precapillary (Ra), postcapillary, or total pulmonary vascular resistance. In patients, an elevated alveolar-arterial oxygen pressure gradient of 50 to 150 torr resulted in significantly increased Ra. Further hypoxemia did not increase this response. In addition, the effective pulmonary capillary pressure did not bear a constant relationship to the pulmonary artery occlusion or wedge pressure (WP). Therefore, in patients in respiratory failure, WP does not reliably estimate hydrostatic pressure at the pulmonary capillaries.     

Echocardiographic evaluation of left and right ventricular diastolic function in patients with chronic obstructive pulmonary disease.

The aim of this study was to investigate the effects of chronic obstructive pulmonary disease (COPD) on left ventricular and right ventricular diastolic and systolic functions. Forty-eight patients with severe COPD were studied. Patients were divided into 2 subgroups according to pulmonary artery pressures: 25 patients with pulmonary hypertension (group 1) and 23 patients with normal pulmonary artery pressure (group 2). As a control group, 59 normal subjects were studied (group 3). Patients in group 1 had higher tricuspid peak A velocity, lower tricuspid E velocity, longer isovolumetric relaxation time, higher mitral A wave, lower mitral E wave, and slower color propagation velocity than groups 2 and 3. There was no significant difference between left ventricular diastolic filling parameters between groups 2 and 3. Patients with COPD and pulmonary hypertension have left and right ventricular diastolic dysfunction. However, patients with COPD and normal pulmonary artery pressure have normal left and right ventricular diastolic function.