Johnson, Bruce D.

ABSTRACT Introduction Regional heterogeneity of the human heart plays an important role in left ventricular (LV) and right ventricular (RV) function and may contribute to enhanced myocardial efficiency in the athlete’s heart. Purpose This study comprehensively characterized regional and transmural myocardial tissue deformation (strain) in recreationally active (RA) and endurance-trained (ET) men to determine if regional nonuniformity evolves alongside morphological adaptations associated with endurance training. Methods Echocardiography was used to measure LV and RV global, regional (apical, mid, basal) and transmural (endocardial, epicardial) longitudinal strain in 30 endurance-trained (ET) (age, 31 ± 2 yr; body mass index, 23.1 ± 0.5 kg·m −2 ; V˙O 2peak , 60.2 ± 6.5 mL·kg −1 ·min −1 ) and 30 RA (age: 29 ± 2 yr; body mass index, 23.4 ± 0.4 kg·m −2 ; V˙O 2peak : 42.6 ± 4.6 mL·kg −1 ·min −1 ). Nonuniformity was characterized using apex-to-base and transmural (endocardial-to-epicardial) strain gradients. Results Global longitudinal strain was similar in ET and RA in the left (−17.4% ± 0.4% vs −17.8% ± 0.5%, P = 0.662) and right ventricle (−25.8% ± 0.8% vs 26.4% ± 1.0%, P = 0.717). The apex-to-base strain gradient was greater in ET than RA in the left (−6.5% ± 0.7% vs −2.7% ± 0.8%, P = 0.001) and right ventricle (−9.6% ± 1.8% vs −3.0% ± 1.6%, P = 0.010). The LV transmural strain gradient was greater than RV in both groups, but similar in ET and RA (−4.7% ± 0.2% vs −4.7% ± 0.2%, P = 0.850), whereas RV transmural strain gradient was greater in ET than RA (−3.4% ± 0.3% vs −1.6% ± 0.4%, P = 0.003). RV apex-to-base and transmural strain gradients correlated with RV end-diastolic area ( R = 0.536 & 0.555, respectively, P < 0.01) and V˙O 2peak ( R = 0.415 & 0.677, respectively, P < 0.01). Conclusions Transmural nonuniformity is more pronounced in the left ventricle than the RV free wall; however, RV functional nonuniformity develops markedly after endurance training. Differences in myocardial architecture and exercise-induced wall stress in the left and right ventricles are possible explanations for the marked functional nonuniformity throughout the myocardium and in response to endurance exercise training.

New Findings What is the topic of this review?This review concerns the negative impact of pulmonary hypertension (PH) on the pulmonary haemodynamic and gas exchange responses to exercise, considering the mechanisms by which PH plays a role in exercise intolerance in heart failure (HF) patients. What advances does it highlight?The hallmark limited pulmonary vascular ‘reserve’ and impaired pulmonary gas exchange responses to exercise in HF are worsened by the development of PH; these are key determinants of exercise intolerance. Even HF patients who present with ‘normal’ pulmonary vascular function experience exercise‐induced PH, which plays a role in exercise intolerance. AbstractPatients with heart failure universally complain of exertional intolerance, but the underlying cause(s) of this intolerance may differ between patients with different disease phenotypes. Exercise introduces an impressive stress to the lungs, where elevations in venous return and cardiac output engender substantial increases in pulmonary blood volume and flow. Relative to healthy individuals, the pulmonary vascular reserve to accept this increase in pulmonary perfusion is compromised in heart failure, with a growing body of evidence suggesting that the development of pulmonary hypertension (PH), and in particular a precapillary component of PH, worsens the pulmonary haemodynamic response to exercise in these patients. Characterized by an exaggerated increase in pulmonary arterial pressure and an elevation in pulmonary vascular resistance, this dysfunctional pulmonary haemodynamic response plays a role in exercise intolerance, probably through an impairment of right ventricular function, underperfusion of the pulmonary circulation and a subsequent reduction in systemic blood flow and oxygen delivery. The hallmark abnormalities in ventilatory and pulmonary gas exchange that accompany heart failure, including a greater ventilatory equivalent for carbon dioxide, are also worsened by the development of PH. This raises the possibility that measures of exercise pulmonary gas exchange might help to ‘describe’ underlying PH in heart failure; however, several fundamental issues and questions need to be addressed before such gas exchange measures could truly be considered efficacious measures used to differentiate the type of PH and track the severity of PH in heart failure.exercise intolerance, heart failure, pulmonary gas exchange, pulmonary haemodynamics, pulmonary hypertension

HeartMate II left ventricular assist device controllers provide data including pulsatility index, reflecting the relationship between pump function and hemodynamics. We propose that a higher pulsatility index at hospital discharge following implant may be associated with less vascular congestion and improved clinical outcomes. A retrospective analysis of 40 patients (age 59.2 ± 10.3 years) supported with the HeartMate II devices was conducted. Data revealed moderate Pearson correlations between pulsatility index at discharge and right atrial pressure, pulmonary artery systolic pressure, pulmonary artery diastolic pressure, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure, respectively, post-surgery (median of 377 days), demonstrating a stronger relationship when analyzed for the EPC controller (n = 28) only (r = −.57, p < .01; r = −.38, p < .05; r = −.59, p < .01; r = −.47, p = .01 and r = −.53, p < .01, respectively). The pulsatility index derived from the EPC controller was associated with the significant risk of re-hospitalization within 1 and 2 years after the implantation of left ventricular assist device; hazard ratio = 0.557 with 95% confidence interval (0.315–0.983), p = .04 and hazard ratio = .579 (0.341–0.984), p = .04. A higher pulsatility index at discharge was associated with greater volume unloading, lower pulmonary pressures, and lower risk of all-cause re-hospitalizations within 1 and 2 years post-surgery. As such, pump-derived data may provide additional value in predicting left ventricular assist device hemodynamics.

Background Detecting significant coronary artery disease (CAD) in the general population is complex and relies on combined assessment of traditional CAD risk factors and noninvasive testing. We hypothesized that a CAD‐specific heart rate variability (HRV) algorithm can be used to improve detection of subclinical or early ischemia in patients without known CAD. Methods and Results Between 2014 and 2018 we prospectively enrolled 1043 patients with low to intermediate pretest probability for CAD who were screened for myocardial ischemia in tertiary medical centers in the United States and Israel. Patients underwent 1‐hour Holter testing, with immediate HRV analysis using the HeartTrends DyDx algorithm, followed by exercise stress echocardiography (n=612) or exercise myocardial perfusion imaging (n=431). The threshold for low HRV was identified using receiver operating characteristic analysis based on sensitivity and specificity. The primary end point was the presence of myocardial ischemia detected by exercise stress echocardiography or exercise myocardial perfusion imaging. The mean age of patients was 61 years and 38% were women. Myocardial ischemia was detected in 66 (6.3%) patients. After adjustment for CAD risk factors and exercise stress testing results, low HRV was independently associated with a significant 2‐fold increased likelihood for myocardial ischemia (odds ratio, 2.00; 95% CI, 1.41–2.89 [ P =0.01]). Adding HRV to traditional CAD risk factors significantly improved the pretest probability for myocardial ischemia. Conclusions Our data from a large prospective international clinical study show that short‐term HRV testing can be used as a novel digital‐health modality for enhanced risk assessment in low‐ to intermediate‐risk individuals without known CAD. Clinical Trial Registration URL: http://www.ClinicalTrials.gov . Unique identifiers: NCT01657006, NCT02201017).

Heart failure (HF) is a complex and multifaceted disease. The disease affects multiple organ systems, including the respiratory system. This review provides three unique examples illustrating how the cardiovascular and respiratory systems interrelate because of the pathology of HF. Specifically, these examples outline the impact of HF pathophysiology on 1) respiratory mechanics and the mechanical “cost” of breathing; 2) mechanical interactions of the heart and lungs; and on 3) abnormalities of pulmonary gas exchange during exercise, and how this may be applied to treatment. The goal of this review is to, therefore, raise the awareness that HF, though primarily a disease of the heart, is accompanied by marked pathology of the respiratory system.

The purpose of this report was to 1) detail the construction of a low-cost device that provides a “reference” flow waveform for pneumotachograph (PNT) calibration, i.e., the “syringe potentiometer” (SP), and to compare the 2) accuracy and 3) practical performance of “calibration curves” obtained with the SP device to other more established methods of PNT calibration, i.e., the weighted averaging (WA) and polynomial least-squares (PolyLS) methods. Volume and flow waveforms obtained via the SP device were validated against a motion capture system and were deemed accurate surrogates of actual syringe volume and flows. The SP device was used to construct a calibration curve of a PNT by dividing the flow waveform of the SP by the analog output of the PNT amplifier. A total of 187 inspiratory and 187 expiratory strokes were collected. When the entire data set of expiratory strokes was used, the SP, WA, and PolyLS methods together demonstrated acceptable volume and flow errors as per American Thoracic Society/European Respiratory Society recommendations (less than ±3.5% and less than ±5.0% errors, respectively). The “practical” performance of each method was assessed with a nested subsampling procedure, whereby volume and flow errors were evaluated as the number of strokes was increased (in blocks of 5 strokes). To this end, the SP method demonstrated practical performance superior to that of the WA and PolyLS approaches, whereby acceptable volume and flow errors were achieved after only 5 calibration strokes; the WA and PolyLS methods required 15 and 20 strokes, respectively, to achieve the same level of volume and flow accuracy.NEW & NOTEWORTHY This report describes the construction and validation of a low-cost device for the purposes of pneumotachograph (PNT) calibration: the “syringe potentiometer” (SP). Calibration of a PNT with the SP device yielded acceptable volume and flow errors (<3.5% and 5%, respectively) across a wide range of flows (<0.5 to 15 L/s). The SP device offered superior “practical performance” over other established PNT calibration methods, whereby acceptable volume and flow errors were achieved after only five calibration strokes.

We propose that abnormalities of the pulmonary system contribute significantly to the exertional dyspnea and exercise intolerance observed in patients with chronic heart failure. Interventions designed to address the deleterious pulmonary manifestations of heart failure may, therefore, yield promising improvements in exercise tolerance in this population.

Introduction: Long-term use of continuous-flow left ventricular assist devices may have negative consequences for autonomic, cardiovascular and gastrointestinal function. It has thus been suggested that non-invasive monitoring of arterial pulsatility in patients with a left ventricular assist device is highly important for ensuring patient safety and longevity. We have developed a novel, semi-automated frequency-domain-based index of arterial pulsatility that is obtained during suprasystolic occlusions of the upper arm: the ‘cuff pulsatility index’. Purpose: The purpose of this study was to evaluate the relationship between the cuff pulsatility index and invasively determined arterial pulsatility in patients with a left ventricular assist device. Methods: Twenty-three patients with a left ventricular assist device with end-stage heart failure (six females: age = 65 ± 9 years; body mass index = 30.5 ± 3.7 kg m −2 ) were recruited for this study. Suprasystolic occlusions were performed on the upper arm of the patient’s dominant side, from which the cuff pressure waveform was obtained. Arterial blood pressure was obtained from the radial artery on the contralateral arm. Measurements were obtained in triplicate. The relationship between the cuff pressure and arterial blood pressure waveforms was assessed in the frequency-domain using coherence analysis. A mixed-effects approach was used to assess the relationship between cuff pulsatility index and invasively determined arterial pulsatility (i.e. pulse pressure). Results: The cuff pressure and arterial blood pressure waveforms demonstrated a high coherence up to the fifth harmonic of the cardiac frequency (heart rate). The cuff pulsatility index accurately tracked changes in arterial pulse pressure within a given patient across repeated measurements. Conclusions: The cuff pulsatility index shows promise as a non-invasive index for monitoring residual arterial pulsatility in patients with a left ventricular assist device across time.