Acute Ventricular Dilatation Research Articles

The risk factors of chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage

Objectives: The purpose of this study was to explore the independent risk factors of chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage. Methods: A retrospective study was carried out in patients with aneurysmal subarachnoid haemorrhage and admitted to the Second Affiliated Hospital of Chongqing Medical University from July 2017 to February 2021. The patients were grouped according to whether they had chronic ventricular dilatation. The patients’ demographic, clinical, and imaging datas including gender, age, hypertension, Hunt and Hess grade, Fisher grade, intraventricular hemorrhage, acute ventricular dilatation, aneurysm location, cerebrospinal fluid drainage, surgical methods, and meningitis were recorded and analyzed. And binary multivariate logistic regression models were used to investigate the independent risks for the chronic ventricular dilatation. Results: A total of 70 patients were analyzed and 36 (51.4%) developed chronic ventricular dilatation. Univariate analysis showed that age, Hunt and Hess grade, Fisher grade, intraventricular hemorrhage, acute ventricular dilatation, subtentorial aneurysms, and cerebrospinal fluid drainage were significantly different between the two groups. And there was no significant difference between the two groups in gender, hypertension, surgical method, or meningitis. Multivariate logistic regression analysis showed that acute ventricular dilatation was the only independent risk factor for chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage (OR 92.1, 95% CI: 11.7–999.9, P < 0.001). Conclusions: Acute ventricular dilatation was an independent risk factor of chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage. Future research is needed to assess whether early treatment of acute ventricular dilatation can reduce chronic ventricular dilatation.

Echocardiographic markers of mortality at 60 days in patients with COVID-19 in the intensive care unit

Abstract Introduction Coronavirus disease (COVID)-19 predominantly produces its effects through lung damage, but an important component of multi-organ dysfunction is cardiac involvement. We have few reports that inform about the behavior of echocardiographic images of patients with the most severe forms of the disease. Purpose The present work aims to identify prognostic markers for 60-day mortality in patients hospitalized in intensive care based on echocardiographic findings. Methodology A single-center retrospective cohort was conducted. Hospitalized patients were included in one of the nine intensive care units for COVID-19 confirmed by RT-PCR from May to October 2020. Patients with previous conditions that determined a limitation of the therapeutic effort, those who died before 24 hours and pregnant women were excluded. Portable echocardiograms were performed by two expert cardiologists following the recommendations for isolation and personal protection. The time to death was evaluated as outcome. A Cox proportional hazards model was constructed, HR and 95% confidence intervals with their p values. The study was approved by the institutional ethics committee. Results Of 326 patients included, 153 patients had an echocardiogram. The mean age was 60.7 years, 47 (30.7%) were female and 67 (44.7%) had positive troponin. 91 patients (59.5%) not survive, the mean long of stay was 8.4 (SD: 4.2) days. 111 (72.5%) had shock, 128 (83.7%) severe ARDS (PaO2 / FiO2 <100 mmHg), 142 (92.8%) required invasive ventilatory support, and 86 (56.2%) acute kidney injury. 27 (17.6%) patients had acute pulmonary embolism, 16 (10.4%) acute myocardial infarction and 9 (5.9%) myocarditis. The mean right ventricular ejection fraction was 37%, TAPSE was decreased in 16 cases (10.4%). 41 cases (26.8%) had right diastolic dysfunction. 34/48 (71%) cases had pulmonary hypertension. The average LVEF was 59.3% and 74 (48.4%) had some left ventricular diastolic dysfunction. 12 (7.8%) had left ventricular segmental wall motion abnormality and 16 (10.4%) had pericardial effusion. Univariate analysis identified TAPSE, PSAP, acute cor pulmonale and right ventricular dilatation as variables related to the outcome of mortality. The multivariate Cox model (Table 2) documented that acute cor pulmonale with a HR of 12.8 (95% CI 3.51 - 46.63, p<0.001) and right ventricular dilation with a HR of 4, 87 (95% CI 1.36–17.46, P 0.016) were associated with mortality. Conclusions In patients hospitalized in the intensive care unit for COVID-19, acute cor pulmonale and right ventricular dilatation behaved as independent predictors of in-hospital death. Funding Acknowledgement Type of funding sources: None. Table 1. Baselines characteristicsTable 2. Multivariate analisys

Abstract W MP92: Role of Lipocalin 2 in Acute Ventricular Dilatation After Intraventricular Hemorrhage

Background: Acute hydrocephalus is a common complication following hemorrhagic stroke. Although recent studies demonstrated that intraventricular hemorrhage (IVH) causes hydrocephalus, the exact mechanism by which hydrocephalus develops after IVH are not well understood. Lipocalin 2 (LCN2), a siderophore-binding protein, is an acute phase protein in the brain. In the present study, we examined the role of LCN2 in ventricular dilatation in a mouse model of IVH. Methods: First, female wild type C57BL/6 mice (WT, n=8) underwent a right intraventricular injection of hemoglobin (25mg/ml, 20 μl). Control mice (n=6) received saline injection. Ventricular volume was measured at 24 hours using magnetic resonance images. Second, female wild type and LCN2-deficient (LCN2-/-) mice had an intraventricular injection of hemoglobin (25mg/ml, n=5 for each; 50mg/ml, 20 μl, n=7 for WT and n=11 for LCN2-/-). They underwent magnetic resonance images at pre surgery and then 24 hours after surgery. All mice were euthanized at 24 hours after surgery. Brains were used for immunohistochemistry, immunofluorescence and Western blotting. Data are expressed as means±SD. P<0.05 was considered statistically significant. Results: In wild type mice, injection of hemoglobin (25 mg/ml) rather than saline resulted in ventricular dilatation at 24 hours (12.5±2.4 vs. 8.6±1.5 mm3 in the control, p<0.01). Western blotting showed that LCN2 was significantly upregulated in the periventricular area after hemoglobin injection (26362±4165 vs. 2780±579 pixels in the control, p<0.01). LCN2 was expressed in astrocytes, whereas its receptor was detected in astrocytes and microglia/macrophages. Hemoglobin-induced ventricle enlargement was less in LCN2-/- mice (p<0.01) as was periventricular microglia activation (p<0.01). At a higher dose (50 mg/ml), hemoglobin resulted in high mortality in WT mice (86%), but much lower mortality in LCN2-/- mice (27%; p<0.05). Conclusions: Our results indicate that LCN2 has a critical role in hemoglobin-induced ventricular dilatation.

Timing Is Everything in Protecting the Heart and Lungs in a “Sympathetic Storm”

Timing Is Everything in Protecting the Heart and Lungs in a “Sympathetic Storm”

The Association of Troponin I Levels with Severity of Obstructive Sleep Apnea Syndrome

Background: As a result of repeated nocturnal hypoxemia, pulmonary arterial vasoconstriction, acute right ventricular dilatation and hypokinesia and myocardial injury may occur in patients with Obstructive Sleep Apnea Syndrome (OSAS). As it is known, Cardiac Troponin I (cTnI) is an important marker of myocardial injury. Objectives: The aim of this study is to investigate the degree of myocardial injury which is created with nocturnal hypoxemia by measuring cTnI levels in patients with OSAS and to evaluate the association between cTnI levels and severity of OSAS. Methods: Seventy-six subjects who had OSAS symptoms were examined with standard polysomnography (PSG) and classified according to their Apnea-Hypopnea Index (AHI). Forty-seven patients with AHI ≥ 5 were considered as OSAS and 29 subjects with AHI 30) OSAS (n:20). Serum cTnI levels were measured twice in all subjects after the PSG. Results: When the levels of cTnI were compared, there was no significant difference between patients and controls (OSAS=3.6 ± 2.7 ng/ml and controls=3.1 ± 1.8 ng/ml, p=0.3). Also no significant difference was detected between mild-moderate OSAS (2.93 ± 1.67 ng/ml), severe OSAS (4.57 ± 3.47 ng/ml) and controls comparing with their cTnI levels (p=0.053). But cTnI levels in severe OSAS patients were significantly higher than controls (p=0.01). According to the logarithmic transformation, log-cTnI was 0.49 ± 0.21 ng/ml and 0.47 ± 0.21 ng/ml in OSAS subjects and controls, respectively (p=0.74). Severe OSAS patients had higher log-cTnI levels (0.59 ± 0.22 ng/ml) than mildmoderate OSAS subjects and controls (p=0.018, f=4.26). There was a positive correlation between AHI and cTnI levels in patients with OSAS (r=0.276, p=0.019, R2=0.076). Conclusion: Cardiac troponin I measurements may be useful to show the degree of myocardial injury in severe OSAS.

Sepsis and Myocardial Depression in a Young Woman

Severe sepsis may be associated with depression of myocardial function, attributed to various inflammatory mediators. Myocardial dysfunction in sepsis is characterized by biventricular failure and complicates usual therapy with high-volume fluid resuscitation and vasopressors. However, in patients who survive septic shock, myocardial dysfunction can improve rapidly. We describe a young woman with septic shock due to Streptococcus pneumoniae, complicated by severe but reversible biventricular dysfunction.

Ventricular interdependence: how does it impact on hemodynamic evaluation in clinical practice?

The left (LV) and right ventricles (RV) are enclosed in a stiff envelope, the pericardium. They have similar enddiastolic volumes, and there is no free space for acute ventricular dilatation within a normal pericardial space. Thus, when RV end-diastolic volume increases owing to increased RV loading, it can only occur at the expense of the space devoted to the left ventricle, which is prevented from dilating to as large an end-diastolic volume as it would otherwise given its distending pressure. From a practical point of view this reduced LV end-diastolic volume is accompanied by decreases in LV diastolic compliance, such that for the same LV distending pressure LV end-diastolic volume is less. This point was described in a previous Physiological Note [1]. LV impaired relaxation by RV enlargement is evidenced by Doppler examination of mitral flow velocity (Fig. 1).

Indications, results, and pitfalls in the surgery of constrictive pericarditis.

Constrictive pericarditis is a rare disease with an often unclear etiology. There may be a long delay between the onset of the underlying disease and the onset of clinical symptoms, which are fatigue, abdominal swelling, peripheral edema and breathlessness. However, if clinically apparent, these symptoms may progress rapidly and severely disable the affected patient. Diagnosis is achieved by the clinical presentation, echocardiography and/or MRI and right heart catheterization. The standard therapy is an extended pericardiectomy to restore an unlimited inflow and outflow as well as an unrestricted diastolic function of both ventricles. The risks of this procedure are related to dense adhesions between the 2 pericardial layers and severe calcifications especially of the epicardium. Incomplete removal results in persistent diastolic restriction while lacerations of the underlying myocardium may lead to diffuse and extensive bleeding and finally to myocardial dysfunction. Also, the postoperative course may be complicated by persistent low output syndrome or acute ventricular dilatation. However, early surgical intervention in the hands of experienced surgeons offers the best prognosis.

Modification of stretch-induced shortening of repolarization by streptomycin in the isolated rabbit heart.

The exact mechanism of mechano-electrical feedback and stretch-induced arrhythmias is unknown, but the role of stretch-activated ion channels and specific calcium channels has been proposed. The aim of the present study was to test the hypothesis that stretch-activated ion channels and not calcium channels contribute to stretch-related alterations of repolarization and that these effects can be neutralized by stretch-activated channel block. We studied the interaction of acute ventricular dilatation and the stretch-activated channel blocker streptomycin and the specific calcium channel blocker verapamil in an isolated retrogradely perfused rabbit heart model in which the left ventricular size is modified by abruptly changing the volume of a fluid-filled balloon placed in the left ventricle. Acute ventricular dilatation led to a rate-dependent decrease in repolarization. The mean effective refractory period (ERP) and monophasic action potential duration (MAP90) for cycle lengths between 300 and 1,000 ms decreased from 174.2+/-9 ms and 178.9+/-7 ms to 161.6+/-11 ms and 169.7+/-5 ms, respectively. Streptomycin (80 microM) inhibited this stretch-related shortening of repolarization (ERP: 175.4+/-8 ms; MAP90: 179.7+/-8 ms, p < 0.05) but had almost no effect on already dilated ventricles. Counteraction of the observed electrophysiologic changes could only be achieved by increasing the streptomycin concentration to 200 microM. Streptomycin nearly completely suppressed stretch-related ectopic ventricular complexes. In contrast, verapamil (1 microM) had no effect on stretch-related changes in repolarization and stretch-induced arrhythmias. The present study indirectly implicates stretch-activated ion channels in the genesis of stretch-related changes in repolarization and arrhythmias. The electrophysiologic changes after ventricular dilatation to a degree that increases left ventricular pressure in a clinically relevant range can be influenced by the stretch-activated channel blocker streptomycin but not by specific calcium channel block. This may have clinically important implications for the development of new antiarrhythmic drugs.

Effect of sustained stretch on dispersion of ventricular fibrillation intervals in normal rabbit hearts.

To determine the effect of acute left ventricular dilatation on refractoriness in normal hearts. During sustained ventricular fibrillation (VF) in isolated perfused hearts, recording of local activation time yields VF intervals which provide an index of local refractoriness. Simultaneous measurement from multiple sites enables study of spatial aspects of changes in refractoriness. We studied the effects of stretch on the magnitude and dispersion of changes in VF interval in 10 isolated, Langendorff-perfused rabbit hearts using a flexible epicardial array containing 240 unipolar electrodes. The left ventricular pressure was increased from 0 to 40 mmHg by inflation of an intraventricular balloon during sustained VF. The current threshold for VF induction fell from 64 +/- 11 mA to 43 +/- 11 mA (mean +/- SE, P < 0.01) following ventricular dilatation. Mean VF interval at 0 mmHg was 79.8 +/- 1.3 ms and fell to 70.2 +/- 1.7 ms (P < 0.01) at 40 mmHg. There was a corresponding increase in dispersion of VF interval (coefficient of variation) from 8.13 +/- 0.8 to 13.3 +/- 0.8 (P < 0.01). There was regional heterogeneity in the areas of greatest reduction in VF interval, which varied between hearts. Following balloon inflation there was an increase in the number of activation waves. Acute ventricular dilatation produces spatially heterogeneous changes in refractoriness which would predispose to the maintenance of reentrant arrhythmias.

Divergent effect of acute ventricular dilatation on the electrophysiologic characteristics of d,l-sotalol and flecainide in the isolated rabbit heart.

The interaction between acute ventricular dilatation (AVD) as one aspect of ventricular dysfunction and Class I and III antiarrhythmic drugs is uncertain. We therefore investigated the effects of AVD on the electrophysiologic properties of d,l-sotalol and flecainide. The isolated rabbit heart was used as a model of AVD. The ventricular size and, therefore, the diastolic pressure were modified by sudden volume changes of a fluid-filled balloon placed in the left ventricle. Pacing was performed alternately using epi- and endocardial monophasic action potential (MAP)-pacing catheters at cycle lengths from 1,000 to 300 msec. d,l-Sotalol (10 microM) resulted in a significant (P < 0.05) lengthening of refractoriness (+13.5% +/- 3.1%), MAP duration (+14.9% +/- 3.2%), and QT interval (+15.5% +/- 4.1%) (mean +/- SEM at 1,000 msec). These effects had a reverse rate-dependence. AVD to a diastolic pressure of 30 mmHg reduced refractoriness and left ventricular MAP duration. In comparison with the control group with the same extent of AVD, d,l-sotalol still led to a significant prolongation of repolarization for all cycle lengths except 300 msec, so that its effects were not absolutely but relatively preserved. In contrast, flecainide (2 microM) had no significant effects on refractoriness or MAP duration. It led to a significant, rate-dependent increase of pacing thresholds (+47.6% +/- 8.2%), prolongation of QRS (+48.8% +/- 5.6%), and conduction time (+78.6% +/- 8.6%) (mean +/- SEM at 300 msec). In the flecainide group, AVD significantly increased the normal rate-dependent prolongation of QRS (+16.7% +/- 5.5%) and conduction time (+17.1% +/- 4.3%). Our data demonstrate that, during AVD, the Class III effect of d,l-sotalol is preserved, whereas flecainide's effect of slowing conduction is exaggerated. This may contribute to flecainide-related proarrhythmia in certain clinical situations.

Electrophysiological effects of acute dilatation in the isolated rabbit heart: cycle length-dependent effects on ventricular refractoriness and conduction velocity.

Acute ventricular dilatation has important electrophysiological effects: Dilatation shortens action potential duration and refractoriness without an apparent effect on conduction velocity. These effects have been implicated as a potential mechanism of arrhythmias in patients with congestive failure. Because the influence of cycle length on these phenomena has not been studied, we examined the effects of dilatation during ventricular pacing at cycle lengths from 1000 to 150 ms. Thin epicardial layers were created in isolated, perfused rabbit left ventricles (n=7). A fluid filled latex balloon was secured in the left ventricle to dilate the left ventricle. Mapping was performed with 248 epicardial electrodes. Longitudinal conduction velocity (76+/-1 cm/s; mean+/-SEM) and transverse conduction velocity (26+/-1 cm/s) were not influenced by dilatation at any cycle length. In contrast, the effects of dilatation in decreasing left ventricular effective refractory period (ERP) were significantly greater at shorter drive cycle lengths: The decrease in ERP was 2+/-2 ms (a 1% change) at a drive cycle length of 1000 ms and 18+/-4 ms (a 20% change) at a drive cycle length of 150 ms. In 10 additional intact, isolated perfused rabbit hearts, dilatation decreased ERP to a greater degree during 250 ms drive cycle length pacing than during pacing at 400 ms (25+/-4 versus 16+/-3 ms; P=.01). Acute dilatation exaggerates the normal rate-dependent shortening of refractoriness but does not influence transverse or longitudinal conduction velocity. This observation suggests that the electrophysiological effects of acute dilatation may be greater during tachycardia than at slower cycle lengths. This may have implications for arrhythmias in patients with congestive heart failure.

Interaction of acute ventricular dilatation and d-sotalol during sustained reentrant ventricular tachycardia around a fixed obstacle.

Antiarrhythmic therapy of ventricular tachycardia is associated with decreased efficacy and increased proarrhythmia in patients with congestive heart failure, but the explanation for these observations is not known. This study examined the interaction of ventricular dilatation and d-sotalol in a model of reentry ventricular tachycardia. Thin epicardial layers of anisotropic myocardium were created in Langendorff-perfused rabbit left ventricles by a cryo procedure. A fluid-filled, latex balloon was secured within the left ventricle to change ventricular volume. Sustained reentrant ventricular tachycardia, around a central cryolesion, was induced by rapid pacing in all preparations (n = 7). Epicardial mapping was performed through 248 electrodes. Single premature beats introduced within the reentry circuit were used to define the excitable gap. Dilatation did not influence ventricular tachycardia cycle length or conduction velocity. A 1.25-mL increase in left ventricular volume widened the excitable gap by 12% (range, 5% to 29%) (P < .001) because of a decrease in myocardial refractoriness. d-Sotalol (final concentration, 10 mg/L) narrowed the excitable gap 18% (range, 7% to 29%) (P = .002) in the undilated left ventricle. d-Sotalol was less effective in the dilated left ventricle, narrowing the excitable gap only 9%, a difference that was not statistically significant. During pacing to induce or terminate tachycardia, tachycardia acceleration was observed significantly more frequently in the dilated than in the undilated ventricle. Ventricular tachycardia acceleration was due to the development of double-wave reentry (two successive waves traveling in the same circuit in the same direction). d-Sotalol, which narrowed the excitable gap, prevented tachycardia acceleration and double-wave reentry. Antiarrhythmic efficacy may be decreased by dilatation because of widening of the initial excitable gap and a decrease in the gap-narrowing effect of these agents. Double-wave reentry, more likely with a widening of excitable gap, may partially explain tachycardia acceleration in the dilated ventricle.

Mechanical correlates of contraction-excitation feedback during acute ventricular dilatation.

The purpose was to examine the mechanical correlates of the electrophysiological changes that occur during acute left ventricular dilatation. Ten isolated, retrogradely perfused, ejecting rabbit hearts were studied. Left ventricular volume was adjusted by varying left atrial perfusion pressure. Left ventricular pressure was measured directly. Changes in left ventricular chamber dimensions at the level of an epicardial electrode were evaluated with two dimensional echocardiography and wall stress was calculated from these measures. Regional left ventricular electrophysiological properties were measured at two left atrial perfusing pressures. Increases in left atrial perfusion pressure resulted in significant increases in left ventricular end diastolic and end systolic pressures, epicardial and endocardial circumference, and wall stress. Only changes in diastolic wall stress correlated with changes in ventricular refractoriness (r = 0.69, p = 0.027). Left ventricular dilatation results in shortening of ventricular refractoriness in the isolated, ejecting rabbit heart. Regional changes in refractoriness are best correlated with changes in wall stress.

Effect of acute ventricular dilatation on fibrillation thresholds in the isolated rabbit heart.

We examined the effects of ventricular dilatation on epicardial refractoriness and ventricular fibrillation threshold (VFT) in the isolated, retrograde-perfused rabbit heart. Ventricular size was modified by acutely changing the volume of a fluid-filled balloon secured within either the left or right ventricle. Left ventricular dilatation (to an end-diastolic pressure of 30-38 mmHg) significantly decreased left ventricular effective refractory period (ERP) and myocardial wavelength (calculated as ERP x conduction velocity). Left VFT (determined by scanning the vulnerable period with a train of pulses) decreased from 6.4 +/- 0.9 to 4.4 +/- 0.5 mA; P < 0.01) with left but not right ventricular dilatation. Right ventricular dilatation was associated with a decrease in the right ventricular ERP and myocardial wavelength, and right VFT decreased from 13.6 +/- 1.8 to 4.1 +/- 0.3 mA (P < 0.01). Changes in VFT correlated with the decrease in local refractoriness and shortening of local excitation wavelength.

Acute ventricular dilatation in adult meningococcal meningitis

Acute ventricular dilatation in adult meningococcal meningitis

Electrophysiological effects of acute ventricular dilatation in the isolated rabbit heart.

We examined the effects of left ventricular dilatation on epicardial pacing threshold, conduction velocity, and effective refractory period (ERP) in the isolated, retrograde perfused rabbit heart. Left ventricular size was modified by acutely changing the volume of a fluid-filled balloon anchored within the vented left ventricle. Increases in left ventricular volume, associated with increases in left ventricular end-diastolic pressure from 0 +/- 1 to 35 +/- 2 mm Hg, were not associated with significant changes in pacing threshold or conduction velocity. The left ventricular ERP decreased significantly with an added volume of 1.5 ml (91.4 +/- 5.5 msec) compared with starting volume (117.7 +/- 3.8 msec, p less than 0.01). Right ventricular ERP did not change significantly with increases in left ventricular volume. The left and right ventricular ERPs were comparable at starting volume (117.7 +/- 3.8 and 117.6 +/- 3.5 msec, respectively; p = NS) but were significantly different with an added volume of 1.5 ml (91.4 +/- 5.5 and 112 +/- 5.6 msec, p less than 0.05). These changes were independent of coronary perfusion pressure and paced cycle length, suggesting that ischemia is an unlikely explanation for the observed effects. Changes in left ventricular volume decreased left ventricular ERP in a regionally heterogeneous manner, increasing the temporal dispersion of recovery over the left ventricle nearly twofold. Induced ventricular arrhythmias (ventricular tachycardia or fibrillation) were significantly more frequent at high (35%) than at low (3%) volumes during left ventricular pacing. We conclude that ventricular dilatation is associated with increased dispersion of refractoriness in this model, a finding that correlates with propensity for reentrant arrhythmias.

Posthemorrhagic hydrocephalus in low-birth-weight infants: Treatment by serial lumbar punctures

We have performed weekly computed tomographic brain scans on 28 surviving low-birth-weight infants with cerebral intraventricular hemorrhage and acute ventricular dilatation. Evolving hydrocephalus was observed in 15 infants. Twelve of the 15 infants were treated by removing large volumes of cerebrospinal fluid with serial lumbar punctures. Arrest in the progression of hydrocephalus was evident in 11 of the 12. Clinical hydrocephalus requiring surgical intervention occurred in one of the treated infants and in all three untreated infants. No complications of serial lumbar punctures were noted, whereas shunt-related morbidity was 100%. Our results suggest that serial lumbar punctures are effective in arresting the development of posthemorrhagic hydrocephalus.

The electrocardiogram in acute pulmonary embolism

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.

Pressure-volume correlates of left ventricular oxygen consumption in the hypervolemic dog.

Volume changes in the intact functioning canine left ventricle were induced by whole blood infusion and were measured by the thermodilution technic. Multiple regression analyses were performed to detect significant correlations between hemodynamic variables and left ventricular oxygen consumption. Hemodynamic variables, in addition to the pressure-time integral, ventricular volume, and ventricular work, included estimates of myocardial stress, force, and shortening. The most significant individual correlates of oxygen consumption were the pressure-time integral ( r =0.91) and ventricular end systolic volume ( r =0.81), whereas the interaction of volume with pressure-time, thus approximating wall stress and force, was the most significant variable overall (r=0.93). A number of multiple linear regression models were tested for the prediction of ventricular oxygen consumption. The equation (model E) with the greatest multiple regression coefficient (R=0.947) included heart rate, pressure-time per beat, pressure-time per minute, end systolic volume, and (end systolic volume) 2/3 as independent variables. A less elaborate regression equation including only pressure-time per minute and end systolic volume as independent variables was, however, nearly as accurate as model E in the prediction of oxygen consumption. The addition of estimates of left ventricular work and shortening to these regression models did not further improve the ability to predict oxygen consumption accurately. The relationships between these hemodynamic variables and ventricular oxygen consumption were not altered by pericardiotomy or catecholamine depletion. In the hypervolumic heart acute ventricular dilatation did not occur following pericardiotomy. The results of this study confirm the postulate that an increase in ventricular volume, as well as pressure, will be accompanied by an increase in ventricular oxygen consumption. This in turn implies a relationship between the wall stress or force generated by the myocardium and the energy requirement of contraction.