Left ventricular myocardial oxygen demand and subclinical dysfunction in patients with severe obesity referred for bariatric surgery

2020 ◽  
Author(s):  
Lisa M.D. Grymyr ◽  
Saied Nadirpour ◽  
Eva Gerdts ◽  
Bjørn G. Nedrebø ◽  
Johannes J. Hjertaas ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Severe Obesity ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Subclinical Dysfunction

scholarly journals P1514 Increased myocardial oxygen demand is associated with impaired left ventricular strain in patients with morbid obesity referred for bariatric surgery

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
L M Grymyr ◽  
S Nadirpour ◽  
E Gerdts ◽  
B G Nedreboe ◽  
J J Hjertaas ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Pulse Pressure ◽  
Systolic Function ◽  
Oxygen Demand ◽  
Wall Stress ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Lv Mass ◽  
Obese Subjects ◽  
Lv Systolic Function

Abstract Background Obesity predisposes for left ventricular (LV) hypertrophy and systolic dysfunction. Higher myocardial oxygen demand in LV hypertrophy is associated with higher risk for cardiovascular events, while the association with LV systolic function has been less explored. Purpose To assess the association of myocardial oxygen demand with LV systolic function in morbidly obese subjects without known heart disease. Methods Clinical and echocardiographic data from 110 obese subjects referred for gastric bypass surgery (mean age 42 ± 11 years, 74% women, mean body mass index [BMI] 41.9 ± 4.8 kg/m², 33% with hypertension, 15% with diabetes) in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study was used. LV function was assessed by ejection fraction (EF) by Simpson"s biplane method and endocardial global longitudinal strain (GLS) by 2D vector velocity imaging using a 16-segment model (Image Arena 4.6, Tomtec, Unterschleissheim, Germany). Myocardial oxygen demand was estimated from LV mass - wall stress - heart rate product according to a previously validated formula. Results Myocardial oxygen demand was higher in men (1884 vs. 1579 x 10³ g x kdyne/cm² x bpm, p < 0.05), and associated with higher BMI (r = 0.24) and pulse pressure (r = 0.28), and with lower EF (r = -0.22) and lower GLS (r = 0.26, all p < 0.05). In multiple regression analysis, higher myocardial oxygen demand was associated with lower LV GLS (Beta = 0.21, p < 0.05) independent of age, gender, BMI, pulse pressure, diabetes, and EF (Table). Conclusion In obese patients without known heart disease referred for bariatric surgery, higher myocardial oxygen demand was associated with lower LV systolic function measured by GLS independent of confounders. Covariates of lower GLS in multivariable Variable β correlation coefficient p LV mass - wall stress - heart rate product (g x kdyne/cm² x bpm x 10³) 0.21 0.04 Age (years) -0.12 0.22 Gender 0.34 <0.01 BMI (kg/m²) 0.25 <0.01 Pulse pressure (mmHg) -0.04 0.71 Diabetes -0.17 0.09 LV EF (%) -0.01 0.90

scholarly journals One-year impact of bariatric surgery on left ventricular mechanics: results from the prospective FatWest study

2021 ◽  
Vol 1 (2) ◽  
Author(s):  
Lisa M D Grymyr ◽  
Saied Nadirpour ◽  
Eva Gerdts ◽  
Bjørn G Nedrebø ◽  
Johannes Just Hjertaas ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Heart Rate ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Rapid Weight Loss ◽  
Obese Patients ◽  
Lv Mass ◽  
Severely Obese ◽  
One Year

Abstract Aims Patients with severe obesity are predisposed to left ventricular (LV) hypertrophy, increased myocardial oxygen demand, and impaired myocardial mechanics. Bariatric surgery leads to rapid weight loss and improves cardiovascular risk profile. The present prospective study assesses whether LV wall mechanics improve 1 year after bariatric surgery. Methods and results Ninety-four severely obese patients [43 ± 10 years, 71% women, body mass index (BMI) 41.8 ± 4.9 kg/m2, 57% with hypertension] underwent echocardiography before, 6 months and 1 year after gastric bypass surgery in the FatWest (Bariatric Surgery on the West Coast of Norway) study. We assessed LV mechanics by midwall shortening (MWS) and global longitudinal strain (GLS), LV power/mass as 0.222 × cardiac output × mean blood pressure (BP)/LV mass, and myocardial oxygen demand as the LV mass-wall stress-heart rate product. Surgery induced a significant reduction in BMI, heart rate, and BP (P < 0.001). Prevalence of LV hypertrophy fell from 35% to 19% 1 year after surgery (P < 0.001). The absolute value of GLS improved by—4.6% (i.e. 29% increase in GLS) while LV ejection fraction, MWS, and LV power/mass remained unchanged. In multivariate regression analyses, 1 year improvement in GLS was predicted by lower preoperative GLS, larger mean BP, and BMI reduction (all P < 0.05). Low 1-year MWS was associated with female sex, preoperative hypertension, and higher 1-year LV relative wall thickness and myocardial oxygen demand (all P < 0.001). Conclusion In severely obese patients, LV longitudinal function is largely recovered one year after bariatric surgery due to reduced afterload. LV midwall mechanics does not improve, particularly in women and patients with persistent LV geometric abnormalities. ClinicalTrials.gov identifier NCT01533142, 15 February 2012.

scholarly journals Levosimendan treatment of severe acute congestive heart failure refractory to dobutamine/milrinone in children

2011 ◽  
Vol 68 (11) ◽  
pp. 979-984
Author(s):  
Sergej Prijic ◽  
Sanja Rakic ◽  
Ljubica Nikolic ◽  
Bosiljka Jovicic ◽  
Mila Stajevic ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Myocardial Contractility ◽  
Severe Heart Failure ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Univentricular Heart ◽  
Dilatative Cardiomyopathy ◽  
Hemodynamic Improvement

Introduction. Levosimendan is a novel positive inotropic agent which, improves myocardial contractility through its calcium-sensitizing action, without causing an increase in myocardial oxygen demand. Also, by opening ATP-sensitive potassium channels, it causes vasodilatation with the reduction in both afterload and preload. Because of the long halflife, its effects last for up 7 to 9 days after 24-hour infusion. Case report. We presented three patients 2, 15 and 17 years old. All the patients had severe acute deterioration of the previously diagnosed chronic heart failure (dilatative cardiomyopathy; univentricular heart with bidirectional Glenn anastomosis and restrictive bulboventricular foramen; bacterial endocarditis on artificial aortic valve with severe stenosis and regurgitation). Signs and symptoms of severe heart failure, cardiomegaly (cardio-thoracic index 0.65) and left ventricular dilatation (end-diastolic diameter z-score 2.6; 4.1 and 4.0) were confirmed on admission. Also, myocardial contractility was poor with ejection fraction (EF - 27%, 25%, 35%), fractional shortening (FS - 13%, 11%, 15%) and stroke volume (SV - 40, 60, 72 mL/m2). The treatment with standard intravenous inotropic agents resulted in no improvement but in clinical deterioration. Thus, standard intravenous inotropic support was stopped and levosimendan treatment was introduced. All the patients received a continuous 24-h infusion 0.1 ?g/kg/min of levosimendan. In a single patient an initial loading dose of 11 ?g/kg over 10 min was administrated, too. Levosimendan treatment resulted in both clinical and echocardiography improvement with the improved EF (42%, 34%, 44%), FS (21%, 16%, 22%) and SV (59, 82, 93 mL/m2). Hemodynamic improvement was registered too, with the reduction in heart rate in all the treated patients from 134-138 bpm before, to less than 120 bpm after the treatment. These parameters were followed by the normalization of lactate levels. Nevertheless, left ventricular end-diastolic diameter did not change after the levosimendan treatment. Conclusion. Our initial experience demonstrates that administration of levosimendan in patients with severe chronic heart failure not responsive to standard intravenous inotropic treatment might result in a significant clinical and hemodynamic improvement and that, in selected patients, it might be life saving. According to our best knowledge patients presented are the first pediatric patients treated with levosimendan in our country.

Intra-aortic balloon counterpulsation in the ICU

2016 ◽  
Author(s):  
Alain Combes ◽  
Nicolas Bréchot
Keyword(s):  
Insertion Site ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Ventricular Afterload ◽  
Retroperitoneal Haemorrhage ◽  
Computer Controlled ◽  
Intra Aortic Balloon Counterpulsation ◽  
Critical Ischaemia ◽  
Balloon Counterpulsation

The intra-aortic balloon pump (IABP) is a mechanical device consisting of a cylindrical polyethylene balloon that sits in the aorta, approximately 2 cm from the left subclavian artery. A computer-controlled console linked to either an electrocardiogramor a pressure transducer inflates the balloon with helium during diastole (counterpulsation) and actively deflates in systole. This results in an increase in coronary artery blood flow and cardiac output, and reduced left ventricular afterload. These actions combine to decrease myocardial oxygen demand and increase supply. Major complications include bleeding at the insertion site and retroperitoneal haemorrhage, critical ischaemia of the catheterized leg, catheter infection, and stroke. IABP duration usually varies from 48 to 72 hours. Weaning from IABP is not well defined; the most common approach is to reduce cycling of inflation to 1:2 or 1:4 for 15 minutes to several hours before device removal.

Sex differences in noninvasive estimates of left ventricular pressure energetics but not myocardial oxygen demand in young adults

2014 ◽  
Vol 8 (4) ◽  
pp. 197 ◽  
Author(s):  
William E. Hughes ◽  
Nicole L. Spartano ◽  
Wesley K. Lefferts ◽  
Jaqueline A. Augustine ◽  
Kevin S. Heffernan
Keyword(s):  
Young Adults ◽  
Sex Differences ◽  
Oxygen Demand ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Myocardial Oxygen Demand

scholarly journals Incomplete functional reverse remodelling of the left ventricle one year after bariatric surgery. Insights from the prospective FatWest study

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
L M D Grymyr ◽  
S Nadirpour ◽  
E Gerdts ◽  
B G Nedreboe ◽  
J J Hjertaas ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Systolic Function ◽  
Oxygen Demand ◽  
Female Gender ◽  
Myocardial Oxygen Demand ◽  
Cardiac Power ◽  
Lv Mass ◽  
Severely Obese ◽  
Lv Systolic Function ◽  
Concentric Geometry

Abstract Background Patients with severe obesity are predisposed to development of left ventricular (LV) hypertrophy with subsequent increased myocardial oxygen demand and impaired myocardial function. Bariatric surgery leads to rapid weight loss and improves cardiovascular risk profile. Purpose To assess whether LV systolic function, wall mechanics, and cardiac power improve 1 year after bariatric surgery. Methods 91 severely obese patients (43±10 years, 70% women, body mass index [BMI] 41.7±4.9 kg/m2, 55% with hypertension, 17% with diabetes mellitus) underwent echocardiography before, 6 and 14 months after Roux-en-Y gastric bypass surgery in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study. We assessed LV systolic function by biplane ejection fraction (EF), LV wall mechanics by midwall shortening (MWS) and global longitudinal strain (GLS), and cardiac power normalized for LV mass by 0.222 x cardiac output x mean blood pressure (BP)/LV mass. Results Surgery induced a significant reduction in BMI, heart rate, systolic BP, and LV mass (Figure 1). Prevalence of LV hypertrophy fell from 34 to 20% 14 months after surgery (p<0.001), while that of concentric geometry remained stable: 8 vs 10% (p=0.36). GLS improved by 28%, however LV EF and MWS did not change (Figure 2). LV power at rest decreased postoperatively, reflecting the lower BP and heart rate, but was unaltered when normalized for LV mass (Figure 2). In backward stepwise multivariate regression analyses, 1 year improvement in GLS was predicted by the systolic BP reduction (p<0.05) (R2 0.73, p<0.001), while low 1-year MWS was independently associated with female gender, concentric geometry and higher myocardial oxygen demand (all p<0.01) (Nagelkerke R2 0.44, p<0.001), and lower 1-year LV power-mass with female gender and LV hypertrophy (p<0.01) (R2 0.24, p<0.001). Conclusion In severely obese patients, LV longitudinal function normalizes 1 year after bariatric surgery, mainly due to the BP reduction. LV midwall mechanics and power do not improve, especially in women and patients with persistent LV geometric abnormalities. FUNDunding Acknowledgement Type of funding sources: None. Figure 1 Figure 2

The Ellestad Protocol

2018 ◽  
pp. 149-159
Author(s):  
Myrvin H. Ellestad ◽  
Gregory S. Thomas
Keyword(s):  
Perceived Exertion ◽  
Diastolic Pressure ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Warm Up ◽  
Case Examples ◽  
St Segment ◽  
Patient Preparation ◽  
Electrocardiogram Ecg

The chapter The Ellestad Protocol reviews the performance of a maximal exercise test from start to finish using the Ellestad protocol as an example. Patient preparation should include caffeine avoidance should a vasodilator myocardial perfusion imaging (MPI) test be necessary secondary to inadequate exercise. A light meal prior to exercise testing is acceptable. The Bruce and Ellestad protocols both begin with a stage each investigator regarded as a warm-up, 3 minutes of exercise at 1.7 mph at a 10% grade. With two minute stages, primarily of increasing grade, the Ellestad protocol is completed approximately one minute earlier than the Bruce protocol. The use of the Borg scale of perceived exertion is helpful in determining a patient’s effort. If ancillary MPI is not being performed, an abrupt stop for a motion-free electrocardiogram (ECG) and then immediately placing the patient supine or semi-supine increases pre-load and, via the law of Laplace, increases left ventricular end-diastolic pressure, myocardial oxygen demand and thus ischemia. ST segment depression is observed earlier in recovery than if a cool-down walk is performed. Case examples are provided.

scholarly journals Clinical Assessment of Ventricular Wall Stress in Understanding Compensatory Hypertrophic Response and Maladaptive Ventricular Remodeling

2021 ◽  
Vol 8 (10) ◽  
pp. 122
Author(s):  
Takeshi Tsuda
Keyword(s):  
Ventricular Remodeling ◽  
Clinical Medicine ◽  
Oxygen Demand ◽  
Left Ventricular Pressure ◽  
Wall Stress ◽  
Left Ventricular ◽  
Feedback Signal ◽  
Myocardial Oxygen Demand ◽  
Ventricular Wall ◽  
Critical Determinant

Ventricular wall stress (WS) is an important hemodynamic parameter to represent myocardial oxygen demand and ventricular workload. The normalization of WS is regarded as a physiological feedback signal that regulates the rate and extent of ventricular hypertrophy to maintain myocardial homeostasis. Although hypertrophy is an adaptive response to increased biomechanical stress, persistent hypertrophic stimulation forces the stressed myocardium into a progressive maladaptive process called ventricular remodeling, consisting of ventricular dilatation and dysfunction in conjunction with the development of myocyte hypertrophy, apoptosis, and fibrosis. The critical determinant of this pathological transition is not fully understood, but an energetic mismatch due to uncontrolled WS is thought to be a central mechanism. Despite extensive basic investigations conducted to understand the complex signaling pathways involved in this maladaptive process, clinical diagnostic studies that translate these molecular and cellular changes are relatively limited. Echocardiographic assessment with or without direct measurement of left ventricular pressure used to be a mainstay in estimating ventricular WS in clinical medicine, but in recent years more and more noninvasive applications with magnetic resonance imaging have been studied. In this review article, basic clinical applications of WS assessment are discussed to help understand the progression of ventricular remodeling.

Assessment of viability

2021 ◽  
pp. 545-564
Author(s):  
Luc A. Pierard ◽  
Paola Gargiulo ◽  
Pasquale Perrone-Filardi ◽  
Bernhard Gerber ◽  
Joseph B. Selvanayagam
Keyword(s):  
Coronary Artery ◽  
Myocardial Dysfunction ◽  
Oxygen Demand ◽  
Close Relation ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Severe Coronary Artery ◽  
Coronary Syndromes ◽  
Artery Disease ◽  
Myocardial Thickening

Ischaemic left ventricular (LV) dysfunction due to coronary artery disease (CAD) is steadily increasing as a consequence of the ageing of the population and of improved survival of patients with acute coronary syndromes and currently represents the first cause of heart failure (HF). Myocardial function is dependent on blood supply, as anaerobic reserve is minimum due to a nearly maximal arteriovenous oxygen extraction. At rest, myocardial blood flow remains normal even in the presence of severe coronary artery stenosis (up to 85% diameter stenosis) by coronary autoregulation. In the presence of transstenotic pressure gradient due to epicardial coronary stenosis, arteriolar dilatation maintains normal myocardial flow at rest but with a progressive reduction in flow reserve. When arteriolar dilatation is maximal, autoregulation is exhausted and myocardial ischaemia develops. The limit of autoregulation depends on myocardial oxygen demand and is influenced by heart rate. Tachycardia increases oxygen demand and supply is reduced because of a decreased diastolic perfusion time. In the presence of acute ischaemia, there is a close relation between subendocardial perfusion and transmural function. Indeed, the contribution of subendocardium to myocardial thickening largely exceeds the contribution of the subepicardium. Akinesia can therefore result from subendocardial ischaemia and transmural ischaemia is not necessary. This chapter looks at how viability of the different techniques for treating myocardial dysfunction is assessed.

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