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PubMed2001

Does the presence of hibernating myocardium in patients with impaired left ventricular contraction affect QT dispersion?

BACKGROUND: Hibernating myocardium is associated with increased cardiovascular events. Increased QT dispersion on the surface electrocardiogram is a marker for serious ventricular arrhythmias. In this study, we determine whether hibernating myocardium is associated with increased QT dispersion in patients with coronary artery disease and impaired left ventricular contraction. METHODS: Positron emission tomography with (13)N-ammonia and (18)F-fluorodeoxyglucose determined the presence of metabolic-perfusion mismatch defect. QT dispersion was measured by means of a digitizing tablet with validated software. QT intervals were measured on two separate occasions by two investigators blinded to the result of the positron emission tomography scans. RESULTS: Forty-two patients with impaired left ventricular contraction were studied. They were divided into two groups: group A was made up of patients with mismatch defects (n = 26) and group B was made up of patients with no mismatch defects (n = 16). The mean (SD) QT dispersion measurements were 61.7 +/- 29.8 ms and 70 +/- 24.6 ms for groups A and B, respectively (not significant). When the patients were divided according to the dominant viability status of the impaired myocardial segment, a similar result was found. The patients whose impaired myocardium was dominantly hibernating (n = 19) had a mean QT dispersion of 66.4 +/- 31.9 ms compared with 63.6 +/- 24.8 ms in the patients whose impaired myocardium was mainly scarred (not significant). CONCLUSIONS: QT dispersion is not affected by the presence of hibernating myocardium and is therefore not clinically useful in identifying patients with this phenomenon. This is in contrast with recent reports by other groups and calls for further investigation of this dichotomy.

Ammonia↗
PubMed1998

Blood flow in myocardial hibernation.

Myocardial hibernation is a state of persistently impaired left ventricular function in patients with coronary artery disease that improves after revascularization. It was thought to be caused by a chronic reduction in resting myocardial blood flow in a segment subtended by a diseased coronary artery. However, recent studies using positron emission tomography have demonstrated that absolute myocardial blood flow (mL/min/g) to hibernating myocardium is within normal limits in most patients. The authors hypothesize that hibernating myocardium may be the result of repetitive myocardial stunning, that is, the reversible contractile dysfunction occurring after an episode of myocardial ischemia despite the return of blood flow to normal. Myocardial stunning has been demonstrated in humans in different clinical settings, and recent studies have provided evidence that repetitive episodes of exercise induced ischemia can lead to cumulative and prolonged left ventricular dysfunction akin to that observed in hibernating myocardium.

Animals↗
PubMedDate not supplied

Myocardial hibernation vs repetitive stunning in patients.

Myocardial hibernation is a state of persistently impaired left ventricular function in patients with coronary artery disease that was thought to be caused by a chronic reduction in resting myocardial blood flow in a segment subtended by a diseased coronary artery. However, recent studies using positron emission tomography have demonstrated that absolute myocardial blood flow (ml/min/g) to hibernating myocardium is within normal limits in most patients. If resting flow is not reduced, one must therefore suspect an alternative "trigger" for hibernation that is still a consequence of coronary artery disease and ischemia. We suspect that hibernating myocardium may be the result of repetitive myocardial stunning. Myocardial stunning is the reversible contractile dysfunction occurring after a period of myocardial ischemia that persists for a period of time despite the return of blood flow to normal. Myocardial stunning has been demonstrated in humans in the setting of thrombolysis, coronary angioplasty, coronary artery bypass surgery, and coronary artery spasm. Furthermore, stunning has been demonstrated after exercise in patients with coronary artery disease, and recent studies have provided evidence that repetitive episodes of exercise-induced ischemia can lead to cumulative and prolonged left ventricular dysfunction.

Coronary Circulation↗
PubMed1995

Hibernating myocardium versus scar: severity of irreversible decreased myocardial perfusion in prediction of tissue viability.

PURPOSE: To determine whether quantitation of the relative severity of decreased perfusion in irreversible defects on myocardial perfusion images enables differentiation of viable hibernating myocardium from scar. MATERIALS AND METHODS: In 145 patients with previous myocardial infarction, 1,252 regions with irreversible defects proved by means of rubidium-82 rest-stress imaging were analyzed for relative severity (percentage decrease in perfusion). Myocardial tissue viability was determined by means of positron emission tomography with fluorine-18 fluorodeoxyglucose (FDG). RESULTS: The relative decreases in Rb-82 uptake in the 1,252 regions were categorized into nine levels of severity (30% to > or = 70%) in 381 regions of hibernating myocardium and 871 regions of scar. The values of relative decreased perfusion in the irreversible defects alone did not enable differentiation of hibernating myocardium and scar (P = .61). CONCLUSION: The results show no relationship between the relative severity of irreversible perfusion defects and the ability to distinguish between hibernating myocardium and scar.

Cell Survival↗
PubMed2000

Less afterload sensitivity in short-term hibernating than in acutely ischemic and stunned myocardium.

Short-term hibernating myocardium is characterized by reduced contractile function during persistent moderate ischemia, the recovery of metabolic parameters, and the absence of necrosis. To study the afterload dependence of regional wall excursion in short-term hibernating myocardium, in 11 enflurane-anesthetized swine the left anterior descending coronary artery was cannulated and hypoperfused for 90 min to reduce anterior systolic wall thickening (WT, sonomicrometry) by 60%. Under control conditions, at 5 and 90 min ischemia the descending thoracic aorta was acutely constricted to increase left ventricular (LV) pressure by 30 mmHg. Under control conditions, increased LV pressure resulted in decreased WT [i.e., a negative slope of the relationship between WT and LV end-systolic pressure: -11.2 +/- 4.2 (SD) microm/mmHg]. This slope was further significantly decreased at 5 min ischemia (-26.5 +/- 8.8 microm/mmHg) but returned toward control values in short-term hibernating myocardium at 90 min ischemia (-17.2 +/- 6.6 microm/mmHg). At 30 min reperfusion, the slope was once more significantly decreased (-27.8 +/- 8.1 microm/mmHg). In conclusion, WT in short-term hibernating myocardium is less afterload dependent than in acutely ischemic and reperfused myocardium.

Acute Disease↗
PubMed2004

Temporal and spatial variations in structural protein expression during the progression from stunned to hibernating myocardium.

BACKGROUND: Dysfunctional and normally perfused remote regions show equal myolysis and glycogen accumulation in pig hibernating myocardium. We tested the hypothesis that these arose secondary to elevations in preload rather than ischemia. METHODS AND RESULTS: Expression of structural protein (desmin, desmoplakin, titin, cardiotin, alpha-smooth muscle actin, lamin-A/C, and lamin-B2) in viable dysfunctional myocardium was analyzed by immunohistochemistry. We performed blinded analysis of paired dysfunctional left anterior descending coronary artery and normal remote subendocardial samples from stunned (24 hours; n=6), and hibernating (2 weeks; n=6) myocardium versus sham controls pigs (n=7). Within 24 hours, cardiac myocytes globally reexpressed alpha-smooth muscle actin. In stunned myocardium, cardiotin was globally reduced, whereas reductions in desmin were restricted to the dysfunctional region. Alterations progressed with the transition to hibernating myocardium, in which desmin, cardiotin, and titin were globally reduced. A qualitatively similar reorganization of cytoskeletal proteins occurred 3 hours after transient elevation of left ventricular end-diastolic pressure to 33+/-3 mm Hg. CONCLUSIONS: Qualitative cardiomyocyte remodeling similar to that in humans with chronic hibernation occurs rapidly after a critical coronary stenosis is applied, as well as after transient elevations in left ventricular end-diastolic pressure in the absence of ischemia. Thus, reorganization of cytoskeletal proteins in patients with viable dysfunctional myocardium appears to reflect chronic and/or cyclical elevations in preload associated with episodes of spontaneous regional ischemia.

Actinin↗
PubMed1993

Dobutamine stress echocardiography identifies hibernating myocardium and predicts recovery of left ventricular function after coronary revascularization.

BACKGROUND: The identification of hibernating myocardium is important in selecting patients who will benefit from coronary revascularization. This study was performed to determine whether dobutamine stress echocardiography (DSE) could identify hibernating myocardium and predict improvement in regional systolic wall thickening after revascularization. METHODS AND RESULTS: DSE was performed in 49 consecutive patients with multivessel coronary disease and depressed left ventricular function. Contractile reverse during DSE was defined by the presence of two criteria: (1) improved systolic wall thickening in at least two adjacent abnormal segments and (2) > or = 20% improvement in regional wall thickening score. Postoperative echocardiograms were evaluated for improved regional wall thickening in 25 patients at least 4 weeks after successful coronary revascularization. All studies were read in blinded fashion. Contractile reserve during DSE was present in 24 (49%) of 49 patients. The presence or absence of contractile reserve on preoperative DSE predicted recovery of ventricular function in the 25 patients who underwent successful revascularization. Thus, 9 of 11 patients with contractile reserve had improved systolic wall thickening after revascularization (hibernating myocardium), whereas 12 of 14 patients without contractile reserve did not improve (P = .003). CONCLUSIONS: Dobutamine stress echocardiography provides a simple, cost-effective, and widely available method of identifying hibernating myocardium and predicting improvement in regional left ventricular wall thickening after coronary revascularization. This technique may be clinically valuable in the selection of patients for coronary revascularization.

Adult↗
PubMed1997

Hibernating myocardium: an incomplete adaptation to ischemia.

BACKGROUND: We tested the hypothesis that hibernating myocardium represents an incomplete adaptation to a reduced myocardial oxygen supply. METHODS AND RESULTS: In 38 patients, areas of hibernating myocardium were identified by angiography, multigated radionuclide ventriculography, thallium scintigraphy with reinjection, and low-dose dobutamine echocardiography. Biopsies removed at cardiac surgery showed structural degeneration characterized by a reduced protein and mRNA expression and disorganization of the contractile and cytoskeletal proteins myosin, actin, desmin, titin, alpha-actinin, and vinculin by electron microscopy, immunohistochemistry, and in situ hybridization. Additionally, an increased amount of extracellular matrix proteins resulting in a significant degree of reparative fibrosis was present. Dedifferentiation, ie, expression of fetal proteins, was absent. Apoptosis indicating suicidal cell death was found by the terminal deoxynucleotidyl transferase end-labeling method and electron microscopy. Radionuclide ventriculography showed improvement of regional function at 3 months postoperatively compared with preoperative values (mean values, 23.5% and 48%, respectively), and the echocardiographic wall-motion score index decreased from 3.4 to 1.8. The degree of severity of the morphological changes (three stages) correlated well with the extent of postoperative functional recovery: more advanced clinical improvement was observed in patients with slight and moderate morphological degeneration (stages 1 and 2), but recovery was only partial in severe degeneration (stage 3). CONCLUSIONS: Cellular degeneration rather than adaptation is present in hibernating myocardium. The consequence is progressive diminution of the chance for complete structural and functional recovery after restoration of blood flow. The practical consequence from this study should be early revascularization in patients showing areas of hibernating myocardium.

Adaptation, Physiological↗
PubMed2003

Hibernating myocardium retains metabolic and contractile reserve despite regional reductions in flow, function, and oxygen consumption at rest.

Hibernating myocardium, characterized by reductions in flow and function at rest, has limited contractile reserve in response to increases in external workload. We hypothesized that this attenuation of function reflects an adaptive downregulation that prevents the development of metabolic evidence of ischemia during stress. To test this hypothesis, pigs were chronically instrumented with a proximal left anterior descending artery stenosis for 3 months, resulting in severe anteroapical hypokinesis with reduced resting perfusion (0.78+/-0.05 versus 0.94+/-0.07 mL x min(-1)x g(-1) in remote, P<0.01; and 0.99+/-0.08 in controls, P<0.05). Open-chest studies confirmed resting dysfunction compared with normal controls (segment shortening 9.2+/-2.2% versus 23.5+/-1.1%, P<0.05). Resting myocardial oxygen consumption was reduced (63+/-3 versus 77+/-6 microL x g(-1) x min(-1) in controls, P<0.05), yet lactate consumption was normal. Although subendocardial perfusion failed to increase during graded, intravenous epinephrine infusion (n=8), peak segment shortening (to 17.3+/-3.1%, P<0.05) and oxygen consumption (to 90+/-6 microL x g(-1) x min(-1), P<0.01) increased from the depressed resting levels. There was no lactate production in hibernating myocardium, and lactate uptake increased during stress (0.7+/-0.1 to 1.2+/-0.1 micromol x g(-1) x min(-1), P<0.05). The absence of metabolic evidence of ischemia was also confirmed during atrial pacing to a rate of 120 bpm (n=8). Thus, despite reductions in function and oxygen consumption at rest, hibernating myocardium retains the ability to increase metabolism without the development of acute ischemia. This supports the hypothesis that the downregulation of oxygen consumption and function in hibernating myocardium is an adaptive response that prevents a supply-demand imbalance during submaximal increases in cardiac workload when coronary flow reserve is limited.

Adaptation, Physiological↗
PubMed2004

Hibernating myocardium: chronically adapted to ischemia but vulnerable to sudden death.

The inability to reproduce spontaneous ventricular fibrillation in an animal model of chronic coronary artery disease has limited advances in understanding mechanisms of sudden cardiac death (SCD). Swine with hibernating myocardium arising from a chronic left anterior descending coronary artery (LAD) occlusion have a high rate of SCD that parallels the poor clinical survival of medically treated patients with hibernating myocardium. Kaplan-Meier analysis (n=426) demonstrated a cumulative mortality of 49% after 5 months that was almost entirely attributable to spontaneous SCD. Using implantable loop recorders, ventricular fibrillation was documented as the arrhythmic mechanism of death in all animals (n=10) and was usually preceded by ventricular tachycardia (n=8). Physiological studies before SCD (n=7) demonstrated total LAD occlusion and collateral-dependent myocardium (n=5), excluding acute occlusion as a major trigger of arrhythmia. The physiological substrate of hibernating myocardium was present before SCD, with reductions in LAD perfusion (SCD 0.79+/-0.13 versus 0.80+/-0.08 mL/min per g) and wall thickening (SCD 28+/-3% versus 22+/-3%) that were similar to survivors (n=14). Triphenyltetrazolium chloride infarcts among animals with SCD were infrequent (4 of 32) and small, averaging 4.6% of LV mass. Histology (n=4) showed postmortem changes but no acute inflammation nor contraction band necrosis. These data support the notion that hibernating myocardium is a pathophysiological substrate at high risk of SCD. This is independent of changes in functional stenosis severity, acute myocardial necrosis, or fibrotic scar. Thus, regional adaptations that promote myocyte survival in the setting of chronic repetitive ischemia result in a substrate with enhanced vulnerability to lethal arrhythmias and SCD.

Adaptation, Physiological↗
PubMed2005

Adenoviral gene transfer of FGF-5 to hibernating myocardium improves function and stimulates myocytes to hypertrophy and reenter the cell cycle.

Fibroblast growth factors (FGFs) have diverse actions on the myocardium but the importance of stimulating angiogenesis versus direct effects of FGFs on cardiac myocytes is unclear. We used intracoronary injection of a replication-deficient adenoviral construct overexpressing FGF-5 (AdvFGF-5) to improve flow and function in swine with hibernating myocardium. Two-weeks after AdvFGF-5 (n=8), wall-thickening increased from 2.4+/-0.04 to 4.7+/-0.7 mm in hibernating LAD regions (P<0.05) whereas remote wall-thickening was unchanged (6.7+/-0.4 to 5.8+/-0.5 mm). This was associated with small increases in resting flow to dysfunctional myocardium, but flow during adenosine was unchanged (LAD 1.45+/-0.27 versus 1.46+/-0.23 mL/min per g and remote 4.84+/-0.23 versus 4.71+/-0.47 mL/min per g, P=NS). Unexpectedly, animals receiving AdvFGF-5 demonstrated a 29% increase in LV mass over the 2-week period (P<0.05 versus untreated animals with hibernating myocardium and normal shams). Histological analysis confirmed profound myocyte cellular hypertrophy in AdvFGF-5 treated myocardium (19.9+/-0.32 versus 15.2+/-0.92 microm in untreated, P<0.001). Myocytes in the proliferative phase of the cell cycle (Ki-67 staining) increased 7-fold after AdvFGF-5 (2,904+/-405 versus 409+/-233 per 10(6) myocyte nuclei in untreated, P<0.05). Myocyte nuclei in the mitotic phase (phosphorylated histone H3 staining) also increased after AdvFGF-5 (127+/-24 versus 35+/-13 per 10(6) myocyte nuclei in untreated, P<0.05). Thus, rather than angiogenesis, stimulation of hypertrophy and reentry of a small number of myocytes into the mitotic phase of the cell cycle are responsible for the effects of AdvFGF-5 on function. Although additional mechanisms may contribute to the improvement in wall-thickening, overexpression of AdvFGF-5 may afford a way to restore function in hibernating myocardium and ameliorate heart failure in chronic ischemic cardiomyopathy.

Adenoviridae↗
PubMed2005

Carvedilol improves myocardial contractility compared with metoprolol in patients with chronic hibernating myocardium after revascularization.

BACKGROUND: We tested the hypothesis of whether carvedilol delays morphologic degeneration and improves functional outcome compared with metoprolol tartrate in patients with hibernating myocardium undergoing surgical revascularization. We have previously shown that patients with chronic hibernating myocardium undergo progressive cellular degeneration and fibrosis. METHODS: Twenty patients with multivessel coronary artery disease revascularization and hibernating myocardium as assessed by technetium-99m perfusion scintigraphy and fluorine-18-fluorodeoxyglucose positron emission tomography were randomized to receive either carvedilol or metoprolol tartrate for at least 2 months before surgery, and this was continued for 7 months postoperatively. Left ventricular ejection fraction and regional wall motion abnormalities were assessed by left ventriculography at baseline and 7 months postoperatively. Intraoperative transmural needle biopsy samples were obtained for microscopic analysis. RESULTS: Postoperatively, the ejection fraction increased from 31% +/- 5% to 44% +/- 4% (P < .005) in the carvedilol group (n = 10), and from 30% +/- 6% to 40% +/- 6% in the metoprolol tartrate group (P < .05 vs preoperatively and vs carvedilol). Wall motion abnormalities in the carvedilol group improved from -2.1 +/- 0.4 to -0.6 +/- 0.5 (P < .05) and from -2.3 +/- 0.5 to -1.6 +/- 0.6 in the metoprolol tartrate group (P < .05 vs preoperatively and vs carvedilol). Microscopic analysis after 72 +/- 18 days of either treatment showed mild cardiomyocyte degeneration and moderate-to-severe fibrosis (28% +/- 7%) in the carvedilol group compared with moderate cardiomyocyte degeneration and moderate-to-severe fibrosis (33% +/- 6%) in the metoprolol tartrate group. Apoptosis, as assessed by the terminal deoxynucleotidyl transferase nick end labeling method, was observed in only 1 patient in each group. CONCLUSIONS: Carvedilol treatment of hibernating myocardium results in improved functional recovery after revascularization compared with metoprolol tartrate, and this might partially be related to reduced cardiomyocyte degeneration.

Adrenergic beta-Antagonists↗
PubMed2000

[Diagnosis of the hibernating myocardium in early stages of heart failure in patients with coronary heart disease].

The paper presents current views on ischemia-reperfusion and mechanisms of its development. Their role in the development of the hibernating myocardium is shown. Possible clinical manifestations of these conditions and currently available diagnostic techniques are assessed. The purpose of the study was to detect the hibernating myocardium in patients with coronary heart disease (CHD) and arterial hypertension (AH). The study enrolled 13 patients with CHD and AH. Myocardial biventricular scintigraphy was conducted in patients before treatment and during acute coronarolytic test. Prior to treatment, all the patients were found to have reversible asynergy, left and right ventricular myocardial hypo- and dyskinesia caused by the hibernating myocardium. The drug test revealed better segmental contractility than the baseline one due to the fact that the function of asynergic segments recovered and fraction ejection increased. The findings suggest that the hibernating myocardium is diagnosed in patients with CHD and AH without myocardial infarction, which is of importance in determining treatment policy and prognosis in these patients.

Coronary Vessels↗
PubMed2000

Myocardial stunning and hibernation in clinical practice.

Myocardial stunning and hibernation are both clinically important causes of myocardial dysfunction and are caused by episodes of myocardial ischaemia. Stunning tends to occur acutely and may produce transient but clinically important reductions in left ventricular function in the setting of myocardial infarction, post coronary artery bypass grafting and even following episodes of effort induced angina. Hibernation refers to a chronic down-regulation of myocardial function in response to chronic myocardial ischaemia. Hibernating myocardium may be present in up to 50% of patients with significantly impaired left ventricular function and evidence of heart failure. Importantly, both these entities can be either prevented or ameliorated by preventing or lessening ischaemic burden. There is also evidence that there may be an overlap between these two entities and that hibernating myocardium may result from repeated episodes of myocardial ischaemia causing chronic stunning.

Angina Pectoris↗
PubMed2001

Hibernating myocardium.

According to estimates, up to 50% of patients with coronary artery disease and impaired left ventricular function have areas of viable myocardium. This dysfunctional, yet viable myocardial tissue, which can improve functionally after myocardial oxygen supply is reestablished, has been called hibernating myocardium. The possible pathophysiological mechanism that leads to hibernating myocardium is controversial: is the phenomenon due to persistent ischemia or is it the result of repetitive episodes of ischemia and reperfusion, such as myocardial stunning? Regardless of the mechanism, the presence of viable myocardial tissue indicates that structural and biochemical cellular changes occur, and the recovery of left ventricular function after revascularization depends on the severity and extent of these changes. Whether these changes reflect a long-lasting state of cellular dedifferentiation, an adaptive process that is reversible, or eventually lead to cellular degeneration has not been determined. Perhaps early detection of hibernating myocardial tissue via noninvasive imaging techniques used to assess contractile response, integrity of the cellular membrane, myocardial metabolism, and myocardial blood flow and subsequent early coronary revascularization may prevent infarction and deterioration in left ventricular function. Knowledge that reversible changes and areas of viable myocardium can occur in patients with left ventricular dysfunction will assist healthcare providers in the care and management of patients with hibernating myocardium.

Coronary Disease↗
PubMed2001

[Three cardiac mysteries--stunning, hibernation and ischemic preconditioning].

BACKGROUND: Cardiovascular research has led to the identification of three new and important phenomena: myocardial stunning, myocardial hibernation, and ischaemic preconditioning. Myocardial stunning is characterised by transient contractile dysfunction that persists after reperfusion despite the absence of irreversible damage and despite restoration of normal or near normal coronary blood flow. Myocardial hibernation is a condition of sustained reduction of contractile function in hypoperfused but viable myocardium, which recovers completely upon reperfusion. Ischaemic preconditioning refers to a phenomenon by which one or more brief periods of myocardial ischaemia increases the ischaemic tolerance against infarction by endogenous adaptive mechanisms. MATERIAL AND METHODS: Current relevant literature obtained through PubMed search is reviewed with emphasis on occurrence of the phenomena, the therapeutic potential, and the underlying mechanisms. RESULTS: Several observations indicate that myocardial stunning, myocardial hibernation, and ischaemic preconditioning may occur in patients with coronary heart disease. Actually, an increasing amount of evidence indicates that these phenomena are of major importance with regard to myocardial ischaemic tolerance. The mechanisms underlying these phenomena are, however, not yet clarified. INTERPRETATION: A better understanding of the mechanisms underlying myocardial stunning, myocardial hibernation, and ischaemic preconditioning may provide a rational basis for development of therapeutic interventions that increase myocardial ischaemic tolerance.

Humans↗
PubMed2004

[Effect of beta-Blocker Bisoprolol on Function of Hibernating Myocardium in Patients With Chronic Heart Failure of Ischemic Etiology].

AIM: To elucidate effect of beta-blocker bisoprolol on hibernating myocardium in patients with congestive heart failure (CHF) of ischaemic etiology without concomitant use of angiotensin converting enzyme inhibitors. MATERIAL AND METHODS: Men (n=21, mean age 51,1+/-2,3 years) with NYHA class II-III congestive heart failure were divided into 2 groups according to results of dobutamine stress-echocardiography: with (group I, n=11), and without (group II, n=10) hibernating myocardium. All patients received bisoprolol (mean daily dose 8.9+/-0.5 mg) for 6 months. RESULTS: In both groups treatment was associated with NYHA class lowering (36.7%, p=0.002, in group 1, and 33.5%, p=0.02, in group II), significant increase of tolerance to physical exercise, improvement of quality of life. Left ventricular ejection fraction significantly increased (+10.5%, p=0.008) in patients with hibernating myocardium and practically did not change in group II (+4,8%, p=0,08). Meanwhile number of normokinetic zones increased by 94,4% in group I (p=0.008) and by 37,5% (p=0,02) in group II. This was associated with reduction of wall motion score index by 10.6%, p=0,009, and 8.2%, p=0,009, respectively. CONCLUSION: These results evidence for efficacy of treatment of patients with heart failure and hibernating myocardium with beta-blocker bisoprolol. In patients with heart failure of ischemic etiology bisoprolol facilitates transition of a part of myocardium from hypokinetic to normokinetic state.

Adrenergic beta-Antagonists↗
PubMed2005

Does electrocardiographic Q wave burden predict the extent of scarring or hibernating myocardium as quantified by positron emission tomography?

BACKGROUND: The extent of Q wave 'burden' on electrocardiograms (ECGs) has not been correlated with the extent of scarring and hibernation as determined quantitatively by positron emission tomography (PET). OBJECTIVE: A retrospective study was performed to identify if ECG Q wave burden predicts the extent of scarring or mismatch (hibernating myocardium) as defined by rubidium-82/F-18 fluorodeoxyglucose PET viability imaging. PATIENTS AND METHODS: Eighty-three consecutive patients with coronary artery disease undergoing rubidium-82/F-18 fluoro-deoxyglucose viability imaging (mean age 67.9+/-11 years, with a mean ejection fraction of 27+/-7%) formed the study population. Resting ECG was interpreted for the presence or absence of Q waves using standard ECG criteria for Q wave myocardial infarction. Patients were divided into two groups based on their Q wave burden on ECG (small to moderate scar: zero to four Q waves; large scar: five or more Q waves). Automated analysis was used to calculate the extent of scarring and mismatch (hibernating myocardium) on PET as a percentage of left ventricular myocardium. Mean PET scar and mismatch scores were calculated for the two groups. RESULTS: The mean PET scar scores were significantly different between the small to moderate ECG scar group (13.9+/-7.3% of the left ventricle) and the large scar group (20.6+/-8.1% of the left ventricle; P=0.001). The mismatch scores for the small to moderate scar group (4.6+/-2.8%) were not significantly different from those of the large scar group (4.05+/-2.8%; P=0.7). CONCLUSIONS: ECG Q wave 'burden' was associated with the presence of scars as defined by PET but did not accurately predict the amount of hibernating myocardium.

Age Factors↗