Variability in Reassessment of Left Ventricular Ejection Fraction After Myocardial Infarction in the Acute Myocardial Infarction Quality Assurance Canada Study.

Importance: Persistently depressed left ventricular ejection fraction (LVEF) after myocardial infarction (MI) is associated with adverse prognosis and directs the use of evidence-based treatments to prevent sudden cardiac death and/or progressive heart failure. Objective: To assess adherence with guideline-recommended LVEF reassessment and to study the evolution of LVEF over 6 months of follow-up. Design, Setting, and Participants: This was a multicenter cohort study at Canadian academic and community hospitals with on-site cardiac catheterization services. Patients with type 1 acute MI and LVEF less than or equal to 45% during the index hospitalization were enrolled between January 2018 and August 2019 and were followed-up for 6 months. Data analysis was performed from May 2020 to September 2021. Exposures: Baseline clinical factors, in-hospital care and LVEF, and site-specific features. Main Outcomes and Measures: The main outcomes were receipt of repeat LVEF assessment by 6 months and the presence of a persistent LVEF reduction at 2 thresholds: LVEF less than or equal to 40%, prompting consideration of additional medical therapy for heart failure, or LVEF less than or equal to 35%, prompting referral for implanted cardioverter defibrillator in addition to medical therapy. Results: This study included 501 patients (mean [SD] age, 63.3 [13.0] years; 113 women [22.6%]). Overall, 370 patients (73.4%) presented with STEMI, and 454 (90.6%) had in-hospital revascularization. The median (IQR) baseline LVEF was 40% (34%-43%). Of 458 patients (91.4%) who completed the 6-month follow-up, 303 (66.2%; 95% CI, 61.7%-70.5%) had LVEF reassessment, with a range of 46.7% to 90.0% across sites (χ213 = 19.6; P = .11). Participants from community hospitals were more likely than those from academic hospitals to undergo LVEF reassessment (73.6% vs 63.2%; χ21 = 4.50; P = .03), as were those with worse LVEF at baseline. Follow-up LVEF improved by an absolute median (IQR) of 8% (3%-15%). However, 103 patients (34.1%) met the definitions of clinically relevant LVEF reduction, including 52 patients (17.2%) with LVEF less than or equal to 35% and 51 patients (16.9%) with LVEF of 35.1% to 40.0%. Conclusions and Relevance: In this cohort study, approximately 1 in 3 patients with at least mild LVEF reduction after acute MI did not undergo indicated LVEF reassessment within 6 months, suggesting that programs to improve the quality of post-MI care should include measures to ensure that indicated repeat cardiac imaging is performed. In those with follow-up imaging, clinically relevant persistent LVEF reduction was identified in more than one-third of patients.

The relationship between left and right pericardial pressures in humans: an intraoperative study.

BACKGROUND: The purpose of this study was to show the similarity between the pericardial constraint over the right and left ventricles of humans at various levels of central venous pressure (CVP) using flat Silastic balloons in the pericardial space during elective cardiac surgery. METHODS: Six subjects (aged 19-76 years) were instrumented with flat, liquid-containing Silastic balloons in the pericardial space during elective cardiac surgery. No subject had valvular disease or right ventricular (RV) hypertrophy. These balloons were positioned to lie over the RV and left ventricular (LV) free walls to measure RV and LV pericardial pressure (P(prv) and P(plv), respectively). Volume loading was achieved by an intravenous infusion of 1 to 2 L of Ringer's lactate or normal saline. Depending on the patient's status during the operative procedure, the mean CVP was increased by 5-10 mm Hg from the baseline postinduction levels. RV and LV pericardial pressures were measured continuously throughout the volume loading. RESULTS: The pooled data from all subjects demonstrate that RV pericardial pressure is equal to LV pericardial pressure over central venous pressures ranging from 4 to 18 mm Hg and that the RV late-diastolic (pre-a-wave) cavitary pressure (P(rv)) correlates with LV pericardial pressure. CONCLUSIONS: Changes in LV pericardial pressure are approximately equal to changes in RV pericardial pressure and RV late-diastolic (pre-a-wave) cavitary pressure is a good predictor of LV pericardial pressure.

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation.

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

Ventricular interaction during mechanical ventilation in closed-chest anesthetized dogs.

The cardiac effects of positive pressure ventilation and positive end-expiratory pressure are incompletely understood. External constraint due to increased intrathoracic pressure decreases left ventricular end-diastolic volume; the effects on venous return and ventricular interaction are less clear. Phasic changes in inferior vena caval flow, end-diastolic ventricular dimensions and output were measured in seven anesthetized, ventilated normal dogs. During inspiration, caval flow, right ventricular diameter and output decreased; end-diastolic transseptal pressure gradient, septum-to-left ventricular free wall diameter, left ventricular area (ie, left ventricular volume index) and output increased despite the decreased sum of the septum-to-free wall diameters. The reverse occurred during expiration. Increased positive end-expiratory pressure decreased the left ventricular area, but the end-expiratory right ventricular diameter was unchanged. At given airway pressures, right ventricular diameter was greater at higher positive end-expiratory pressures, suggesting that a leftward septal shift (direct ventricular interaction) added to the effect of external constraint on left ventricular end-diastolic volume. In conclusion, positive pressure ventilation reduced right ventricular end-diastolic volume during inspiration and increased the transseptal pressure gradient, which shifted the septum rightward, increasing left ventricular end-diastolic volume and output. The reverse occurred during expiration. Positive end-expiratory pressure constrained left ventricular filling and decreased left ventricular end-diastolic volume further by a leftward septal shift.

Atrioventricular nonuniformity of pericardial constraint.

Physiologists and clinicians commonly refer to "pressure" as a measure of the constraining effects of the pericardium; however, "pericardial pressure" is really a local measurement of epicardial radial stress. During diastole, from the bottom of the y descent to the beginning of the a wave, pericardial pressure over the right atrium (P(pRA)) is approximately equal to that over the right ventricle (P(pRV)). However, in systole, during the interval between the bottom of the x descent and the peak of the v wave, these two pericardial pressures appear to be completely decoupled in that P(pRV) decreases, whereas P(pRA) remains constant or increases. This decoupling indicates considerable mechanical independence between the RA and RV during systole. That is, RV systolic emptying lowers P(pRV), but P(pRA) continues to increase, suggesting that the relation of the pericardium to the RA must allow effective constraint, even though the pericardium over the RV is simultaneously slack. In conclusion, we measured the pericardial pressure responsible for the previously reported nonuniformity of pericardial strain. P(pRA) and P(pRV) are closely coupled during diastole, but during systole they become decoupled. Systolic nonuniformity of pericardial constraint may augment the atrioventricular valve-opening pressure gradient in early diastole and, so, affect ventricular filling.

Opening the pericardium during pulmonary artery constriction improves cardiac function.

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.

Evidence for left ventricular constraint during open heart surgery.

BACKGROUND: The degree to which the lungs and other mediastinal structures constrain the heart during cardiac surgery is uncertain. OBJECTIVES: To assess the degree of constraint to left ventricular (LV) filling that is present during cardiac surgery. PATIENTS AND METHODS: Central venous (CVP) and pulmonary capillary wedge pressures (PCWP), and an index of LV end-diastolic volume (LVEDV) - LV area, transesophageal echocardiography - were measured before and after sternotomy, after volume loading, after pericardiotomy, and before and after sternal closure following the clinically indicated procedure in 12 patients undergoing cardiac surgery. PCWP and estimated transmural LVEDP (PCWP-CVP) were plotted against the LV area. RESULTS: In all patients, the difference between PCWP and estimated transmural LVEDP-LV area relations over the full range of LV areas was substantial, indicating the presence of important constraint to filling. Even at small LV areas, when transmural LVEDP approached zero, PCWP was almost always greater than 10 mmHg. Because transmural LVEDP approached zero when areas were smallest, transmural LVEDP-LV area relations were judged to be more plausible than the corresponding PCWP-LV area relations. CONCLUSIONS: Considerable constraint to cardiac filling is effected by the lungs and other mediastinal structures. This constraint must be considered when assessing LV filling pressure - PCWP is not a reliable measure of LV preload in these circumstances.