Significance of Persistent Left Ventricular Dysfunction During Recovery After Dobutamine Stress Echocardiography

Tsoukas, Athanasios; Ikonomidis, Ignatios; Cokkinos, Philip; Nihoyannopoulos, Petros

doi:10.1016/s0735-1097(97)00226-x

Cited by 47 publications

(21 citation statements)

References 23 publications

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“…The fact that these investigators showed a mismatch between function (depressed) and coronary perfusion (restored) further supports the concept that relatively brief episodes of demand-induced ischemia can result in stunned myocardium in humans. Recently, other forms of stress testing have been shown to cause stunning in 74,75 Stunned myocardium most certainly occurs after reperfusion for acute myocardial infarction, but this picture is complicated by a heart that contains both irreversibly injured cells (necrosis) and cells that have been reversibly injured by ischemia/reperfusion, the salvaged myocardium. The analysis by Reimer and Jennings 76 showed that after an abrupt coronary artery occlusion, there is a progressive wave front of cell death in the left ventricle that moves across the wall of the heart from the subendocardial to subepicardial layer (see Figure 1).…”

Section: Clinical Evidence For Stunned Myocardiummentioning

confidence: 99%

Consequences of Brief Ischemia: Stunning, Preconditioning, and Their Clinical Implications

2001

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Abstract-In experimental studies in the dog, total proximal coronary artery occlusions of up to 15 minutes result in reversible injury, meaning that the myocytes survive this insult. The 15 minutes of ischemia, however, induce numerous changes in the myocardium, including certain monuments to the brief episode of ischemia that may persist for days. One of these monuments is stunned myocardium, which represents "prolonged postischemic contractile dysfunction of myocardium salvaged by reperfusion." The mechanism of stunning involves generation of oxygen radicals as well as alteration in calcium homeostasis and possibly alteration in contractile protein structure. Stunning has been observed in several clinical scenarios, including after percutaneous transluminal coronary angioplasty, unstable angina, stressinduced ischemia, after thrombolysis, and after cardiopulmonary bypass. Oxygen radical scavengers and calcium channel blockers have been shown to enhance function of stunned myocardium in experimental studies, and in a few clinical studies, calcium channel blockers have been shown to ameliorate stunning. Although brief periods of ischemia can contribute to prolonged left ventricular dysfunction and even heart failure, they paradoxically play a cardioprotective role. Episodes of ischemia as short as 5 minutes, followed by reperfusion, protect the heart from a subsequent longer coronary artery occlusion by markedly reducing the amount of necrosis that results from the test episode of ischemia. This phenomenon, called ischemic preconditioning, has been observed in virtually every species in which it has been studied and is a powerful cardioprotective effect. The mechanism of ischemic preconditioning involves both triggers and mediators and involves complex second messenger pathways that appear to involve such components as adenosine, adenosine receptors, the epsilon isoform of protein kinase C, the ATP-dependent potassium channels, as well as others, including a paradoxical protective role of oxygen radicals. Both an early and a late phase of preconditioning have been described, and the mechanisms underlying their induction are under investigation. That preconditioning may occur in humans is suggested by the observations that repetitive balloon inflations in the coronary artery are associated with progressively less chest pain, ST-segment elevation, lactate production, the protective effects of preinfarction angina, the anginal "warm-up phenomenon," and studies performed on human cardiac biopsies that show metabolic properties suggesting preconditioning. Development of pharmacological agents that stimulate second messenger pathways thought to be involved in preconditioning, but without causing ischemia, could result in novel approaches to treating ischemia. Hence, on one hand, brief episodes of ischemia can have a negative effect on the heart: stunning; and on the other hand, they have a protective effect: preconditioning. The future challenge is how to minimize the stunning phenomenon and maximize the preconditioni...

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Section: Clinical Evidence For Stunned Myocardiummentioning

confidence: 99%

Consequences of Brief Ischemia: Stunning, Preconditioning, and Their Clinical Implications

2001

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“…4 Furthermore, an important advantage of these tracers over thallium 201 is the possibility of repeating the scan acquisition in case of major patient motion or other causes of inadequate image quality, without the risk of changes in perfusion. The duration of stress-induced functional impairment is controversial, [5][6][7][8][9][10] and scanty data are available about the time course of functional changes after exercise in gated SPECT poststress images. 3 It is therefore unclear what the rate of missed functional ischemic changes would be if the poststress acquisition had to be delayed (eg, because of persistent high subdiaphragmatic activity) or repeated (eg, because of excessive patient motion).…”

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confidence: 99%

Influence of the postexercise acquisition delay on the detection of functional abnormalities in sestamibi-gated SPECT

Sciagrà

Sotgia

Dona

et al. 2007

Journal of Nuclear Cardiology

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Background. Gated single photon emission computed tomography (SPECT) identifies functional changes produced by ischemia, but the influence of acquisition delay on their detection is not established.Methods and Results. In 80 patients with known or suspected coronary artery disease, gated SPECT was acquired twice: first, less than 30 minutes after peak exercise (stress 1), and second, more than 45 minutes after peak exercise (stress 2). End-diastolic volume (EDV), end-systolic volume (ESV), and ejection fraction (EF) were compared with perfusion. The relationship between the ⌬EF (stress EF ؊ resting EF) and the summed difference score (SDS) was ؊0.443 (P < .0001) for stress 1 and ؊0.416 (P < .0001) for stress 2. In stress 1, EF increased in patients without inducible ischemia (SDS ‫؍‬ 0) (57% ؎ 10% vs 54% ؎ 9% at rest, P < .02) and decreased in those with an SDS of 1 or greater (53% ؎ 10.8% vs 55% ؎ 9.6% at rest, P < .05). In stress 2, EF was unchanged in patients without ischemia (55.8% ؎ 9.7%, P ‫؍‬ .06) and decreased in the other patients (52.8% ؎ 10.2%, P < .01). In patients without ischemia, both the EDV and ESV decreased significantly in stress 1 and were unchanged in stress 2. In patients with an SDS of 1 or greater, the EDV remained unchanged and the ESV minimally decreased in stress 1, whereas both volumes clearly and significantly increased in stress 2.

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“…Previously, Tsoukas et al [15] studied the presence of myocardial ischaemia during the recovery phase of DSE. Their results showed that patients with extensive coronary artery disease have more prolonged ischaemia.…”

Section: Discussionmentioning

confidence: 99%

Myocardial viability estimation during the recovery phase of stress echocardiography after acute beta‐blocker administration

Karagiannis

Feringa

Bax

et al. 2007

European J of Heart Fail

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Background: Myocardial viability assessment in severely dysfunctional segments by dobutamine stress echocardiography (DSE) is less sensitive than nuclear scanning. Aim: To assess the additional value of using the recovery phase of DSE after acute beta-blocker administration for identifying viable myocardium. Methods: The study included 49 consecutive patients with ejection fraction (LVEF) ≤ 35%. All patients underwent DSE evaluation at lowhigh dose and during recovery phase, and dual-isotope single photon emission tomography (DISA-SPECT) evaluation for viability of severely dysfunctional segments. Patients with ≥ 4 viable segments were considered viable. Coronary revascularization followed within 3 months in all patients. Radionuclide evaluation of LVEF was performed before and 12 months after revascularization. Results: Viability with DISA-SPECT was detected in 463 (59%) segments, while 154 (19.7%) segments presented as scar. The number of viable segments increased from 415 (53%) at DSE to 463 (59%) at DSE and recovery, and the number of viable patients increased from 43 to 49 respectively. LVEF improved by ≥5% in 27 patients. Multivariate regression analysis showed that, DSE with recovery phase was the only independent predictor of ≥ 5% LVEF improvement after revascularization (OR 14.6,. Conclusion: In this study, we demonstrate that the recovery phase of DSE has an increased sensitivity for viability estimation compared to low-high dose DSE.

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Significance of Persistent Left Ventricular Dysfunction During Recovery After Dobutamine Stress Echocardiography

Cited by 47 publications

References 23 publications

Consequences of Brief Ischemia: Stunning, Preconditioning, and Their Clinical Implications

Consequences of Brief Ischemia: Stunning, Preconditioning, and Their Clinical Implications

Influence of the postexercise acquisition delay on the detection of functional abnormalities in sestamibi-gated SPECT

Myocardial viability estimation during the recovery phase of stress echocardiography after acute beta‐blocker administration

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