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PubMed1987

[Mid-term outcome of acute right ventricular dysfunction in biventricular myocardial infarction. Hemodynamic and cineangiographic studies].

This study was designed to evaluate the mid-term outcome of the right ventricular (RV) dysfunction which characterizes infarction of both ventricles in the acute phase. Thirteen patients hospitalized for inaugural posterior or infero-posterior infarction extending to the right ventricle (haemodynamic and cineangiographic diagnosis) were explored in the acute phase and 4 months later by right heart catheterization and selective cineangiography of the right ventricle in a 30 degrees RAO projection. The results were compared with those obtained in a control group. Haemodynamically, the RV filling pressures (p less than 0.001) and the indices of RV dysfunction--i.e. RV end-diastolic pressure/RV systolic pressure ratio (p less than 0.001) and right atrial pressure/pulmonary wedge pressure ratio (p less than 0.02)--were significantly decreased between the acute and chronic phases, but they remained pathological compared with those measured in the control group. Angiographically, the right ventricular dysfunction in the acute phase was reflected in an increase of the RV end-systolic volume (p less than 0.02) and a decrease of the RV ejection fraction (p less than 0.01), whereas diastolic cavitary dilatation was inconstant, with mean values of RV end-diastolic volume close to those found in the control group. The systolic dysfunction persisted, unchanged, during the chronic phase. Segmental kinetics of the inferior wall was much reduced in the acute phase (p less than 0.001), this hypokinesia partially regressing in the chronic phase; but in fact there were wide individual variations, and some patients even recovered an almost normal contractility. Tricuspid valve regurgitation was frequent (6/13 cases) in the acute phase and regressed in 2 out of 3 cases in the chronic phase; its presence introduced a degree of bias in the measurement of RV end-systolic volume and RV ejection fraction, with a tendency to underestimate the severity of diastolic dysfunction. To summarize, right ventricular dysfunction was constant but often modest in the acute phase and remained relatively stable at mid-term, whereas segmental kinetics of the inferior wall improved, sometimes dramatically.

Adult↗
PubMed1993

Activation of neurohumoral systems in postinfarction left ventricular dysfunction.

OBJECTIVES: This study was conducted to evaluate the degree of neurohumoral activation around the time of hospital discharge after myocardial infarction. BACKGROUND: Because pharmacologic interventions that block the effects of neurohumoral activation improve the prognosis after infarction, we hypothesized that widespread neurohumoral activation persists in some patients until at least the time of hospital discharge and that the determinants of activation vary from one system to another. METHODS: Five hundred nineteen patients in the Survival and Ventricular Enlargement Study (SAVE) had plasma neurohormones measured before randomization at a mean of 12 days after infarction. All patients had left ventricular dysfunction (left ventricular ejection fraction < or = 40%) but no overt heart failure. RESULTS: Although all neurohormones except epinephrine were increased compared with values in age-matched control subjects, plasma norepinephrine (301 +/- 193 vs. 222 +/- 87 pg/ml, p < 0.001), renin activity (3.0 +/- 3.7 vs. 1.2 +/- 1.2 ng/ml per h, p < 0.001), arginine vasopressin (1.9 +/- 6.9 vs. 0.7 +/- 0.3 pg/ml, p < 0.001) and atrial natriuretic peptide (75 +/- 75 vs. 21 +/- 9 pg/ml, p < 0.001) values ranged from normal to very high, indicating a wide spectrum of neurohumoral activation. Activation of one system did not correlate with activation of another. The clinical and laboratory variables most closely associated with neurohumoral activation were Killip class, left ventricular ejection fraction, age and use of diuretic drugs. The association between neurohumoral activation and clinical and laboratory variables varied from one neurohormone to another. CONCLUSIONS: Neurohumoral activation occurs in a significant proportion of patients at the time of hospital discharge after infarction. Which neurohormone is activated and which clinical and laboratory variables determine this activation vary from one neurohormone to another.

Aged↗
PubMed1991

[Relaxation and diastolic filling precisely evaluated in patients with left ventricular dysfunction].

To assess left ventricular (LV) diastolic function in patients with LV dysfunction, LV pressures (manometer tip) and biplane angiograms were analyzed for 27 patients with LV systolic dysfunction (EF < or = 0.45) (dilated cardiomyopathy or coronary artery disease) and 18 normal controls. LV volumes were obtained from frame-by-frame analyses of angiograms. LV relaxation was assessed by the time constant (T) of LV pressure decay. LV relaxation was impaired in patients with LV dysfunction, however, early diastolic filling assessed by the peak filling rate (PFR) and mean filling rate (MFR) during the rapid filling phase was maintained. Compared to the control group, early diastolic filling was significantly decreased in patients with LV dysfunction without mitral regurgitation (MR), but not in those with LV dysfunction with MR. In conclusion, although diastolic filling may be modified by MR, LV relaxation and early diastolic filling are essentially impaired in patients with LV dysfunction.

Adolescent↗
PubMed1987

Antiarrhythmic efficacy and hemodynamic effects of cibenzoline in patients with nonsustained ventricular tachycardia and left ventricular dysfunction.

This was a prospective single-blind, placebo-controlled study of cibenzoline in 21 patients with five or more runs of nonsustained ventricular tachycardia (VT) and left ventricular dysfunction (mean left ventricular ejection fraction 36 +/- 24%). Ambulatory electrocardiographic monitoring revealed a baseline of 616 +/- 431 runs of VT/day on placebo. Of the 18 patients tolerating the drug, 14 (77%) patients initially had a 75% or greater reduction in VT (177 +/- 164 runs of VT/day, p less than .05). A repeat ambulatory electrocardiogram documented long-term suppression of VT in 13 of 14 patients at 1 month (2.1 +/- 1.3 runs VT/day, p less than .01), in 10 of 14 patients at 3 months (2.5 +/- 1.9 runs VT/day, p less than .01), and in nine of 14 patients at 6 months (1.5 +/- 0.8 runs VT/day, p less than .01). Aggravation of arrhythmia or drug failure was seen in four of 18 (22%) patients (new onset of sudden cardiac death, two patients; sustained VT, two patients). Hemodynamic measurements were obtained with the use of right heart catheterization in patients at rest and exercising during the placebo phase and after 60 hr of oral cibenzoline. Group hemodynamic variables, both measured and derived, showed no detrimental effect of cibenzoline. However, in three of 21 patients (mean ejection fraction 21%), cibenzoline was discontinued due to severe depression of left ventricular function. Caution is recommended in the use of cibenzoline in patients with left ventricular ejection fractions of less than 25%.

Aged↗
PubMed1991

Does ventricular dysfunction occur during liver transplantation?

In conclusion, we believe that ventricular dysfunction occurs infrequently during liver transplantation, except for the very short period of "cardioplegia" of the heart on reperfusion in some patients. There is no evidence that prolonged cardiac dysfunction is a common problem during liver transplantation. Understanding the physiologic changes that occur during liver transplantation should allow the anesthesiologist to correct many factors that might otherwise cause hemodynamic instability.

Heart Diseases↗
PubMed1989

[Successful repair of tetralogy of Fallot with severe right ventricular dysfunction using veno-arterial bypass in an adult].

A 35-year-old male with tetralogy of Fallot, who had undergone left Blalock-Taussig shunt at ten year old, developed severe dysfunction of right ventricle with decreased right ventricular ejection fraction of 25% and frequent premature ventricular contractions of right ventricular origin. Following intracardiac procedure, the venoarterial assist circulation was successfully employed for 9 hours, until his hemodynamic conditions were improved. This experience reemphasized the importance of right ventricular protection and mechanical circulatory assist in the surgical treatment of Fallot's tetralogy in older children and adults who developed severe right ventricular dysfunction as a natural history of this disease.

Adult↗
PubMed2001

[ACE inhibition in patients with myocardial infarct and ventricular dysfunction: inappropriate application of therapy standards in patient samples].

Several reports indicate the benefit of ACE inhibitors for patients with left ventricular systolic dysfunction after acute myocardial infarction (MI). We sought to determine the implementation of the treatment guidelines in patient samples from the general population. Furthermore we aimed to identify patient characteristics associated with the use of ACE inhibitors. Screening of two MI-registries allowed the identification of 226 MI patients with left ventricular dysfunction. Patients were considered to be eligible for ACE inhibitor therapy when a EF < or = 40% was documented in the patient records of cardiac rehabilitation clinics (REG-MI, n = 147) or detected by standardised echocardiography (KORA, n = 78). On average 5.5 years following MI, a standardised questionnaire and a detailed medical history was obtained. Specifically, information was collected regarding current medication and potential contraindications for ACE inhibitors. MI patients with LV dysfunction received ACE inhibitors in 62% (REG-MI) and 45% (KORA). The doses prescribed were substantially smaller than target doses used in the large-scale studies (REG-MI: 40 +/- 4%, KORA: 23 +/- 3%, % of target doses). Only 13% (REG-MI) and 3% (KORA) received more than 50% of the target dosage. Additionally, actual doses of the most frequently used ACE inhibitors were significantly different (captopril: 23 +/- 2%, enalapril: 42 +/- 5% of target doses). The likelihood of receiving ACE inhibitors was significantly higher in patients with written recommendation for such medication (odds ratio 6.02, confidence interval 1.93-20.16) and in patients visiting cardiologists (odds ratio 3.69, confidence interval 1.26-11.07) as revealed by multivariate analysis of the REG-MI database. Despite national and international guidance, a large proportion of MI patients with left ventricular dysfunction is not receiving ACE inhibitors, and when used, the doses prescribed are markedly smaller than target doses used in clinical trials that established the utility of these drugs. Medical care by cardiologists and written recommendation of ACE inhibition in patient records were independent predictors of a more appropriate prescription of ACE inhibitors.

Aged↗
PubMed1998

Prognostic value of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease and left ventricular dysfunction. Investigators of this Multicenter Study.

OBJECTIVES: The purpose of our study was to assess the prognostic importance of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease (CAD) and left ventricular (LV) dysfunction. BACKGROUND: The amount of dysfunctional but viable myocardium predicts the functional improvement after revascularization and may offer more precise risk stratification of patients referred for bypass surgery or coronary angioplasty. METHODS: Two hundred and seventy-four consecutive patients with CAD and LV ejection fraction < or =40% underwent low-dose dobutamine echocardiography for viability assessment. One hundred and thirty-three of them were revascularized using either coronary artery bypass surgery (118 patients) or coronary angioplasty (15 patients) and entered this study. To quantify the amount of dysfunctional but viable myocardium, wall motion was scored using 16-segment model. The dysfunctional segments were defined as viable if they exhibited improvement in their thickening by at least 1 grade with dobutamine infusion. The patients were followed up for a mean period of 20+/-12 months (range, 2 to 48) for cardiac mortality and nonfatal cardiac events including myocardial infarction, unstable angina pectoris requiring hospitalization and hospitalization for heart failure. Standard follow-up echocardiography was performed 3 to 6 months after revascularization. RESULTS: Twenty-nine patients exhibited a large amount of dysfunctional but viable myocardium (> or =6 segments, group A), 60 patients had a small amount of dysfunctional but viable myocardium (2 to 5 segments, group B) and 44 patients were found to have dysfunctional myocardium irreversibly damaged (group C). Similar prerevascularization LV ejection fractions of 35%+/-5%, 34%+/-4%, 36%+/-4% in groups A, B and C increased to 47%+/-6% (p < 0.01 vs. baseline, p < 0.01 vs. groups B and C), to 40%+/-5% (p < 0.01 vs. baseline) and to 37%+/-6% (p = NS vs baseline), respectively, after revascularization. The greatest functional improvement after revascularization in group A patients was accompanied by a lower rate of cardiac events during follow-up (2 vs. 18 in group B, p < 0.05, and vs. 17 in group C, p < 0.01) and better cardiac event-free survival according to Kaplan-Meier survival analysis (p < 0.05 vs. groups B and C, respectively). CONCLUSION: In revascularized patients with CAD and moderate or severe LV dysfunction, the presence of a large amount of dysfunctional but viable myocardium identifies patients with the best prognosis.

Adult↗
PubMed1982

The stunned myocardium: prolonged, postischemic ventricular dysfunction.

Myocardial ischemia has, for many decades, been viewed as an all-or-none process that causes myocardial necrosis when prolonged and severe, but whose effects are transient when it is brief or mild. In view of the evidence that the ischemic process may "hit, run and stun," perhaps our thinking about the consequences of myocardial ischemia should be expanded. According to this formulation, an ischemic insult not of sufficient severity of duration to produce myocardial necrosis may acutely affect myocardial repolarization and cause angina (hit); but these changes wane rapidly (run), when the balance between myocardial oxygen supply and demand has been reestablished. However, the ischemia may interfere with normal myocardial function, biochemical processes and ultrastructure for prolonged periods (stun). The severity and duration of these postischemic changes depend on the length and intensity of the ischemia, as well as on the condition of the myocardium at the onset of the ischemic episode. Furthermore, it is likely that when the myocardium is repeatedly stunned, it may exhibit chronic postischemic left ventricular dysfunction, an ill-defined condition. If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardial perfusion by surgical treatment.

Adenosine Triphosphate↗
PubMed2003

Non-transplant surgery for heart failure and severe left ventricular dysfunction. Opportunities and limitations.

The need of alternatives to transplantation has lead to routinely reconsidering conventional surgery for selected patients with advanced heart failure. Although the recovery of ventricular contractility with revascularization sometimes restores ventricular function almost to normality while dramatically enhancing the quality of life, only a few patients with ischemic left ventricular dysfunction exhibit the amount of hibernating myocardium required for such a spectacular outcome taking place. Advanced remodeling is a further obstacle and is currently being addressed by means of operations designed to reduce ventricular volume and restore geometry. Hemodynamic measurements raise concerns, however, as to the diastolic function and the competence of the mitral valve late after reconstructive surgery. Finally, the repair of mitral valve regurgitation has produced interesting short-to-medium term results both in terms of survival and heart failure relief. Yet, their durability is uncertain, if not disappointing when the valvular disease has an ischemic etiology. Expectations of patients undergoing one of the aforementioned procedures, or a combination thereof, should not be averaged as they heavily depend on the specific patient profile under evaluation.

Cardiac Surgical Procedures↗
PubMed1996

Metoprolol abolishes exercise-induced left ventricular dysfunction in patients with silent ischemia.

Left ventricular systolic function is reduced during episodes of silent ischemia in patients with coronary artery disease (CAD). Left ventricular ejection fraction (LVEF) is increased at least 5 absolute percent during exercise in most normal subjects; however, in patients with CAD, LVEF often remains unchanged or decreases. The anti-ischemic effect of beta-adrenergic receptor blockade is well documented, including a reduction of exercise-induced electrocardiographic ST depressions; however, the effect of these drugs on left ventricular volume changes during exercise in patients with silent ischemia is unknown. The aim of this study was to evaluate the effect of a cardio-selective beta-blocking agent, metoprolol, on rest and exercise LVEF in patients with silent ischemia, using radionuclide cardiography. Fifteen patients with silent ischemia completed a double-blind, placebo-controlled crossover study at rest and during submaximal exercise. LVEF remained unchanged during exercise in the placebo phase (56% to 58%; p = NS), but even though LVEF tended to decrease 56% during rest after metoprolol versus 52% after placebo (p = NS), the LVEF increase from rest to exercise resembled a normal LVEF response, 52% to 58% (p = 0.005). Exercise-induced electrocardiographic ST depressions were also reduced during metoprolol treatment. In patients with silent ischemia, the exercise-induced change in LVEF rises significantly during metoprolol treatment. The mechanism may be a reduction in myocardial ischemia as indicated by a reduction in ischemic electrocardiographic findings.

Adrenergic beta-Antagonists↗
PubMed2002

Extracorporeal membrane oxygenation for unprotected left main stenting in a patient with totally occluded right coronary artery and severe left ventricular dysfunction.

We report a case of unprotected left main stenting in an elderly female with severe left ventricular dysfunction and a totally occluded right coronary artery using hemodynamic support with the Extracorporeal Membrane Oxygenator (ECMO). There were no procedural complications and at 6-month follow-up, the patient was doing well with no cardiovascular events. Stenting of unprotected left main and the use of ECMO in high-risk coronary intervention are reviewed.

Aged↗
PubMed1997

Comparison of mortality rates and progression of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy and dilated versus nondilated right ventricular cavities.

This study assesses the influence of right ventricular (RV) dilation on the progression of left ventricular (LV) dysfunction and survival in patients with idiopathic dilated cardiomyopathy (IDC). Using transthoracic echocardiography, we studied 100 patients with IDC aged 20 to 80 years (mean 55 +/- 14); 67% were men. In the apical 4-chamber view, diastolic LV and RV chamber area measurements classified patients into 2 groups: group RV enlargement+ (RV area/LV area > 0.5) included 54 patients; group RV enlargement- (no RV enlargement) had RV area/LV area < or = 0.5. Echocardiographic studies were repeated in all patients after a mean of 33 +/- 16 months. At the time of the initial study, the 2 groups did not differ in age, gender, incidence of atrial fibrillation and diabetes, left ventricular mass, and LV ejection fraction, but the RV enlargement+ group had more severe tricuspid regurgitation and less LV enlargement. After 47 +/- 22 months (range 12 to 96), patients in group RV enlargement+ had lower LV ejection fraction (29% vs 34%, p = 0.006) than patients with initial RV enlargement-. At clinical follow-up, mortality was higher (43%) in patients with initial RV enlargement+ than the RV enlargement- patients (15%), p = 0.002. For survivors, the mitral deceleration time averaged 157 +/- 36 ms; for nonsurvivors or patients who required transplant, the mitral deceleration time averaged 97 +/- 12 ms (p < 0.0001). With use of a multivariate Cox model adjusting for LV ejection fraction, LV size, and age, the relative risk ratio of mortality from initial RV enlargement+ was 4.4 (95% confidence limits 1.7 to 11.1) (p = 0.002). Thus, patients with significant RV dilation had nearly triple the mortality over 4 years and more rapidly deteriorating LV function than patients with less initial RV dilation. In IDC, RV enlargement is a strong marker for adverse prognosis that may represent a different morphologic subset.

Adult↗
PubMed2000

Diffuse and severe left ventricular dysfunction induced by epicardial coronary artery spasm.

Endothelial dysfunction and effectiveness of treatment of calcium antagonists are suggestive of coronary artery spasm as an underlying disorder in dilated cardiomyopathy (DCM). The aim of this study is to determine whether or not the epicardial coronary artery spasm can induce severe cardiac dysfunction like DCM. Thirty-four consecutive patients with angiographically normal coronary arteries and diffuse left ventricular hypokinesis whose causes had been unknown underwent acetylcholine provocation test and left ventricular biopsy. Eight patients were excluded according to the clinical and laboratory data and biopsy findings suggesting myocarditis or other systemic diseases. According to the results of the acetylcholine provocation test, 17 patients were finally diagnosed as having DCM, and nine patients (35% of the study patients), who had acetylcholine-induced diffuse and multivessel coronary spasm, were diagnosed as having DCM-like vasospastic angina pectoris (VSA). Clinical and cardiac catheterization data including hemodynamics and biopsy findings were similar between the two groups except that left ventricular end-systolic volume was significantly greater in DCM than in DCM-like VSA. After the acetylcholine provocation test, DCM patients received both a beta blocker and an angiotensin-converting enzyme inhibitor, and DCM-like VSA patients received antianginal drugs. In echocardiographic findings at predischarge and those after 6-month drug treatment, both DCM-lke VSA and DCM showed significant reduction in end-diastolic and end-systolic diameters and significant increase in fractional shortening and ejection fraction, whereas changes in ejection fraction and fractional shortening were significantly greater in DCM-like VSA than those in DCM. Epicardial coronary artery spasm can induce diffuse and severe left ventricular dysfunction like DCM in VSA. Although antianginal drugs markedly improve left ventricular function of these patients, only the acetylcholine provocation test can identify DCM-like VSA.

Acetylcholine↗
PubMedDate not supplied

Using a 6-minute walk test to predict outcomes in patients with left ventricular dysfunction.

Maximal oxygen consumption (VO2MAX) is an independent variable that predicts outcomes in patients suffering from left ventricular dysfunction (LVD). Determining VO2MAX in a rehabilitation setting is not only costly and time-consuming but it would also be beyond many patients' physical abilities. This study's goal was to show that a simpler and less costly 6-minute walk test can predict mortality in patients with LVD. Sixty-six Phase 1 cardiac rehabilitation patients with LVD performed the 6-minute walk test upon admission and at discharge from a rehabilitation hospital. Upon discharge, the group that was able to walk significantly longer distances upon discharge had a higher survival rate 3 months after discharge. The 6-minute walk test can predict longer survival in patients with LVD and can provide valuable information for determining treatment plans, future prognosis, and home disposition of deconditioned LVD patients in a rehabilitation setting.

Aged↗
PubMed2002

[Clinical evaluation of the cause of left ventricular dysfunction in type 2 diabetes without significant cardiac disease].

OBJECTIVES: The relationship between left ventricular dysfunction and hypertension or proteinuria was evaluated in type 2 diabetic patients without significant cardiac disease to investigate the cause of diabetic cardiac dysfunction. METHODS: Twenty-one patients with type 2 diabetes mellitus (mean age 63.8 +/- 7.4 years) underwent left ventriculography and Doppler echocardiography to calculate the ejection fraction and E/A ratio (E/A). RESULTS: Thirteen patients had hypertension (61.9%) and six patients had proteinuria (28.6%). The E/A was 0.82 +/- 0.21 in all patients. The E/A in patients with hypertension or proteinuria was significantly less than in those without these diseases (0.74 +/- 0.18 vs 0.97 +/- 0.18, p = 0.011; 0.65 +/- 0.10 vs 0.89 +/- 0.20, p = 0.010, respectively). The ejection fraction was 73.3 +/- 7.2% in all patients. The ejection fraction in patients with proteinuria was significantly less than in those without proteinuria (67.6 +/- 10.0% vs 75.5 +/- 4.4%, p = 0.019), but there was no significant difference in ejection fraction between patients with and without hypertension. The duration of diabetes was significantly related to the ejection fraction (r = -0.436, p = 0.048) but not to the E/A. CONCLUSIONS: In patients with type 2 diabetes without significant cardiac disease, left ventricular diastolic function may be related to both hypertension and proteinuria and left ventricular systolic function may be related to proteinuria and duration of diabetes. Therefore, in addition to hypertension, complications of nephropathy or long duration of diabetes may be related to the cause of the diabetic cardiac dysfunction.

Diabetes Mellitus, Type 2↗
PubMed1992

Chronic coronary artery constriction leads to moderate myocyte loss and left ventricular dysfunction and failure in rats.

Coronary artery narrowing, ranging from 19% to 61%, was induced in rats and ventricular performance, myocardial damage, and myocyte hypertrophy were examined 1 mo later. Animals were separated into two groups, exhibiting ventricular dysfunction and failure, respectively. Dysfunction consisted of a 2.4-fold increase in left ventricular end diastolic pressure (LVEDP), 15% decrease in left ventricular peak systolic pressure (LVPSP), 24% reduction in developed pressure (DP), and a 16% depression in-dP/dt. Failure was defined on the basis of a 4.7-fold elevation in LVEDP, and a 26%, 47%, 45%, and 41% decrease in LVPSP, DP, +dP/dt, and -dP/dt. Moreover, in this group, right ventricular end diastolic and systolic pressures increased 5.5- and 1.2-fold. Left and right ventricular weights expanded 23% and 51% with dysfunction and 30% and 56% with failure. Left ventricular hypertrophy was characterized by ventricular dilation and wall thinning which were more severe in the failing animals. Foci of damage were found in both groups but tissue injury was more prominent in the endomyocardium and in failing rats. Finally, myocyte loss in the ventricle was 10% and 20% with dysfunction and failure whereas the corresponding enlargements of the unaffected myocytes were 34% and 53%. Thus, coronary narrowing led to abnormalities in cardiac dynamics with an increase in diastolic wall stress and extensive ventricular remodeling in spite of a moderate loss of myocytes and compensatory reactive hypertrophy of the viable cells.

Animals↗
PubMed1999

Attenuation correction improves the detection of viable myocardium by thallium-201 cardiac tomography in patients with previous myocardial infarction and left ventricular dysfunction.

The aim of this study was to determine the influence of attenuation-corrected thallium-201 stress/redistribution/reinjection single-photon emission tomography (SPET) on the number of viable segments in patients with previous myocardial infarction and dysfunctional myocardium. Fifty-one patients with previous myocardial infarction and left ventricular dysfunction were included in the study. In all patients, 201Tl non-corrected (NC) and attenuation-corrected (AC) SPET was performed using a stress/redistribution/reinjection protocol followed by coronary angiography. A semiquantitative analysis was performed using polar maps for NC and AC stress, redistribution and reinjection short-axis and vertical long-axis (apex) slices. Severe (perfusion defect below 50%/maximal count rate: PD < 50), mild and moderate persistent defects for redistribution and reinjection were evaluated for both NC and AC studies. A total of 1581 segments were evaluated by semiquantitative segmental analysis for both NC and AC studies for each redistribution and reinjection map. In the redistribution maps, NC revealed a total of 352 segments and AC a total of 222 segments with impaired perfusion below 50% of the maximal count rate (PD < 50). The mean number of affected segments was 6.9 +/- 5.5 in the case of NC and 4.4 +/- 4.8 in the case of AC (P < 0.001). In the reinjection maps, NC revealed a total of 263 non-viable segments (PD < 50) and AC a total of 169 non-viable segments. The mean number of affected segments was 5.2 +/- 5.3 in the case of NC and 3.3 +/- 4.2 in the case of AC (P < 0.001). Recovery of function was better predicted by AC than by NC in 20% of patients in the follow-up group. Therefore, the use of attenuation correction influences the extent of viable segments by showing more viable segments in either redistribution or reinjection maps. 201Tl imaging without attenuation correction may underestimate the extent of tissue viability, which may contribute to the lower sensitivity compared to fluorine-18-fluorodeoxyglucose positron emission tomography, where attenuation correction is a routinely performed procedure.

Exercise Test↗