Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia

Markham, Roy V.; Winniford, Michael D.; Firth, Brian G.; Nicod, Pascal; Dehmer, Gregory J.; Lewis, Samuel E.; Hillis, L.David

doi:10.1016/0002-9149(83)90192-3

Cited by 55 publications

(5 citation statements)

References 36 publications

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“…In this group, we could not exclude the presence of ischemia. We chose not to incorporate either ST-segment depression or chest pain into our classification, as they may be seen as an artifact of rapid pacing/tachycardia and hence lack sensitivity and specificity for diagnosing cardiac ischemia in this context(16,24–26). Finally, we did not include a control group that did not undergo pacing, and thus cannot completely exclude cardiac injury caused by placement of the pacing catheter as a source for troponin release.…”

Section: Discussionmentioning

confidence: 99%

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Myocardial Ischemia Induced by Rapid Atrial Pacing Causes Troponin T Release Detectable by a Highly Sensitive Assay

Turer

Addo

Martin³

et al. 2011

Journal of the American College of Cardiology

138

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Objectives The purpose of this study was to assess whether (1) very small increases in troponin T, measured by a new highly sensitive assay for cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis and (2) serial changes can discriminate ischemia from other causes of cTnT release. Background A new hs-cTnT assay offers greater sensitivity than current assays. Methods Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple timepoints during and after incremental rapid atrial pacing. cTnT was quantified using a standard and pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary atherosclerosis and myocardial lactate release with pacing. Results cTnT concentrations in CS blood increased from a median of 6.8 to 15.6pg/mL 60-minutes after termination of rapid atrial pacing (p<0.0001), changes that were mirrored at 180-minutes in peripheral blood (5.1 to 11.8pg/mL p<0.0001)]. Although peripheral cTnT concentrations tended to be higher at 180-minutes following pacing for patients with atherosclerosis and lactate elution (n=7) when compared to those without either marker (n=5) (25.0 vs. 10.2pg/mL, p=0.10), relative (1.7- vs 5.2-fold) and absolute (6.8 vs 8.8pg/mL, p=0.50) changes were similar between groups. Conclusions Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive atherosclerosis. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.

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Section: Discussionmentioning

confidence: 99%

“…During ischemia, areas of ischemic myocardium elute lactate from the anaerobic metabolism of pyruvate. As previously reported(14–16), net myocardial lactate elution was defined as [arterial lactate concentration] - [coronary sinus lactate concentration] < 0…”

Section: Methodsmentioning

confidence: 99%

Myocardial Ischemia Induced by Rapid Atrial Pacing Causes Troponin T Release Detectable by a Highly Sensitive Assay

Turer

Addo

Martin³

et al. 2011

Journal of the American College of Cardiology

138

View full text Add to dashboard Cite

show abstract

“…Next, unambiguously defining coronary ischemia is difficult based on any one or several clinical or biochemical parameters. Chest pain and EKG changes are non-specific [16]. Net coronary sinus lactate elution is relatively specific but cardiac glycolysis can be effected by co-morbid conditions, such as diabetes [17], and detection of net lactate efflux may not be sensitive to small areas of myocardial ischemia.…”

Section: Discussionmentioning

confidence: 99%

Increases in Myocardial Workload Induced by Rapid Atrial Pacing Trigger Alterations in Global Metabolism

et al. 2014

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ObjectiveTo determine whether increases in cardiac work lead to alterations in the plasma metabolome and whether such changes arise from the heart or peripheral organs.BackgroundThere is growing evidence that the heart influences systemic metabolism through endocrine effects and affecting pathways involved in energy homeostasis.MethodsNineteen patients referred for cardiac catheterization were enrolled. Peripheral and selective coronary sinus (CS) blood sampling was performed at serial timepoints following the initiation of pacing, and metabolite profiling was performed by liquid chromatography-mass spectrometry (LC-MS).ResultsPacing-stress resulted in a 225% increase in the median rate·pressure product from baseline. Increased myocardial work induced significant changes in the peripheral concentration of 43 of 125 metabolites assayed, including large changes in purine [adenosine (+99%, p = 0.006), ADP (+42%, p = 0.01), AMP (+79%, p = 0.004), GDP (+69%, p = 0.003), GMP (+58%, p = 0.01), IMP (+50%, p = 0.03), xanthine (+61%, p = 0.0006)], and several bile acid metabolites. The CS changes in metabolites qualitatively mirrored those in the peripheral blood in both timing and magnitude, suggesting the heart was not the major source of the metabolite release.ConclusionsIsolated increases in myocardial work can induce changes in the plasma metabolome, but these changes do not appear to be directly cardiac in origin. A number of these dynamic metabolites have known signaling functions. Our study provides additional evidence to a growing body of literature on metabolic ‘cross-talk’ between the heart and other organs.

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“…Table 2 Group changes in regional ejection fraction. However, it is generally accepted that the appearance of regional wall-motion abnormalities is a sensitive marker of regional myocardial ischaemia (Markham et al, 1983), although other possibilities including metabolic disturbances are conceivable. As coronary angiograms were not available in our study, we could not tell if regional hypokinesia was anatomically associated with coronary lesions.…”

Section: Haemodynamic Responsesmentioning

confidence: 99%

“…As coronary angiograms were not available in our study, we could not tell if regional hypokinesia was anatomically associated with coronary lesions. However, it is generally accepted that the appearance of regional wall-motion abnormalities is a sensitive marker of regional myocardial ischaemia (Markham et al, 1983), although other possibilities including metabolic disturbances are conceivable.…”

Section: Haemodynamic Responsesmentioning

confidence: 99%

Acute effects of smoking on left ventricular function and neuro‐humoral responses in patients with known or suspected ischaemic heart disease

Høilund‐Carlsen

Marving

Gadsbøll³

et al. 2004

Clin Physio Funct Imaging

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Systolic left ventricular function was examined by radionuclide ventriculography in 12 habitual smokers with known or suspected ischaemic heart disease, aged 33-69 years, before, during, and after smoking of two cigarettes in a row and was repeated on a non-smoking control day. Plasma concentrations of adrenaline, noradrenaline, renin, and angiotensin II were determined on the smoking day, before and immediately after smoking. During smoking, there were significant increases in heart rate (+27%), rate-pressure product (+23%), and cardiac output (+14%) in the face of a significant increase in left ventricular end-systolic volume (+5%) and significant decreases in ejection fraction (-6%) and stroke volume (-8%). Blood pressure was virtually unchanged, and total peripheral resistance remained constant. Plasma adrenaline increased by 100%, renin decreased by 21%, and noradrenaline and angiotensin II did not change. The humoral changes were not correlated to changes in any of the haemodynamic variables. Areas of myocardial hypokinesis emerged or widened during smoking in 11 of 12 patients. Thus, in patients with known or suspected ischaemic heart disease, smoking was associated with an acute decrease in systolic ventricular function and development of widespread hypokinesis despite adrenaline stimulation.

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Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia

Cited by 55 publications

References 36 publications

Myocardial Ischemia Induced by Rapid Atrial Pacing Causes Troponin T Release Detectable by a Highly Sensitive Assay

Myocardial Ischemia Induced by Rapid Atrial Pacing Causes Troponin T Release Detectable by a Highly Sensitive Assay

Increases in Myocardial Workload Induced by Rapid Atrial Pacing Trigger Alterations in Global Metabolism

Acute effects of smoking on left ventricular function and neuro‐humoral responses in patients with known or suspected ischaemic heart disease

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