Myocardial ischemia and previous infarction contribute to left ventricular dyssynchrony in patients with coronary artery disease.

AIMS: The aim of this study was to characterize determinants of left ventricular mechanical dyssynchrony (LVMD) in patients with coronary artery disease (CAD). METHODS: Medical records and results of myocardial perfusion SPECT/CT studies were evaluated in 326 patients with previously diagnosed CAD. LVMD was assessed with the phase analysis of ECG-gated myocardial SPECT. Dyssynchrony was described with phase histogram bandwidth (PHBW), standard deviation (PHSD) or entropy (PHE) values above limit of the highest normal. RESULTS: Prevalence of LVMD was 29% in CAD patients. Size of the infarction scar and ischemia extent correlated significantly with PHBW, PHSD and PHE (P < 0.001 for all). Independent predictors of LVMD were myocardial infarction scar (P = 0.004), ischemia extent (P = 0.003), and QRS duration (P = 0.003). Previous percutaneous coronary intervention and coronary artery bypass grafting did not independently predict dyssynchrony. CONCLUSIONS: Almost one-third of CAD patients had significant LVMD. Dyssynchrony was associated with earlier myocardial infarction and presence of myocardial ischemia. Previous percutaneous coronary intervention and coronary artery bypass grafting did not independently predict dyssynchrony.

Electrical and mechanical dyssynchrony in patients with right bundle branch block.

BACKGROUND: Though fairly benign reputation, the right bundle branch block (RBBB) can cause left ventricular mechanical dyssynchrony (LVMD). Still, the relationship between electrical disturbance and LVMD is partly unclear among these patients. METHODS: Thirty patients with RBBB and 60 matching controls were studied with vector electrocardiography and myocardial perfusion imaging phase analysis. RBBB group was divided into those with and those without LVMD. RESULTS: Prevalence of LVMD among RBBB patients was 50% and among controls 22%. Odds ratio (OR) for LVMD in patients with RBBB vs controls without RBBB was 3.6 (95% CI 1.4 to 9.3). Ejection fraction (EF), end-systolic volume, the angle between QRS and T vectors, and the QRS angle in the sagittal plane were significantly different between RBBB patients with and without LVMD. The QRS duration was comparable in these groups. EF associated independently with LVMD, explaining 60% of its variation. A cut-off value of EF ≤ 55% detected LVMD in 100% specificity (sensitivity of 47%). CONCLUSION: Half of the patients with RBBB had LVMD. The OR for LVMD between RBBB and normal ECG was 3.6. It seems that EF, rather than electrical parameters, is the main determinant of LVMD. This information might be useful when evaluating indications for cardiac resynchronization therapy.

Relationships between electrical and mechanical dyssynchrony in patients with left bundle branch block and healthy controls.

BACKGROUND: Abnormal electrical activation may cause dyssynchronous left ventricular (LV) contraction. In this study, we characterized and analyzed electrical and mechanical dyssynchrony in patient with left bundle branch block (LBBB) and healthy controls. METHODS: Myocardial perfusion imaging (MPI) data from 994 patients were analyzed. Forty-three patient fulfilled criteria for LBBB and 24 for controls. Electrical activation was characterized with vector electrocardiography (VECG) and LV function including mechanical dyssynchrony with ECG-gated MPI phase analysis. RESULTS: QRS duration (QRSd; r = 0.69, P < .001) and a few other VECG parameters correlated significantly with phase bandwidth (phaseBW) representing mechanical dyssynchrony. End-diastolic volume (EDV; r = 0.59, P < .001), ejection fraction and end-systolic volume correlated also with phaseBW. QRSd (ß = 0.47, P < .001) and EDV (ß = 0.36, P = .001) were independently associated with phaseBW explaining 55% of its variation. Sixty percent of patients with LBBB had significant mechanical dyssynchrony. Those patients had wider QRSd (159 vs 147 ms, P = .013) and larger EDV (144 vs 94 mL, P = .008) than those with synchronous LV contraction. Cut-off values for mechanical dyssynchrony seen in patients with LBBB were QRSd ≥ 165 ms and EDV ≥ 109 mL. CONCLUSIONS: Despite obvious conduction abnormality, LBBB is not always accompanied by mechanical dyssynchrony. QRSd and EDV explained 55% of variation seen in phaseBW. These two parameters were statistically different between LBBB cases with and without mechanical dyssynchrony.

Cardiac remodelling in association with left ventricular dyssynchrony and systolic dysfunction in patients with coronary artery disease.

BACKGROUND: In patients with coronary artery disease (CAD), ischaemic cardiomyopathy may result in progressive cardiac remodelling and left ventricular (LV) dysfunction. Myocardial perfusion imaging (MPI) can be used to quantify LV size and shape, mechanical dyssynchrony (LVMD) and ejection fraction (EF) as well as myocardial ischaemia and injury extents. We investigated the prevalence of LV remodelling (LVR) in patients with CAD and the relationship between LVR, LVMD and EF. METHODS: Three hundred twenty-six patients with CAD were evaluated. The EF and end-diastolic volume (EDV) were measured using MPI. LVMD was assessed using phase analysis. LVR was characterised according to LV dilatation or increased shape indices (systolic shape index [SIES] and diastolic shape index [SIED]). RESULTS: LVR were observed in 41% of CAD patients. EDV, SIES and SIED were larger in patients with LVMD or low EF. After adjustment for age, sex and infarct and ischaemia extents, phase histogram bandwidth correlated with EDV (r = 0.218) and SIES (r = 0.266) and EF correlated with EDV (r = -0.535), SIES (r = -0.554) and SIED (r = -0.217, p < 0.001 for all). CONCLUSIONS: LVR is frequently seen in patients with CAD and may be detected even before the development of symptomatic heart failure. A large LV volume and a more spherical-shaped LV were associated with LVMD and low EF, highlighting the close relationships between remodelling and systolic dyssynchrony and dysfunction. MPI is useful for assessing LVR by providing information about LV size and shape, which changes from an ellipsoid towards a spherical form in the development of ischaemic cardiomyopathy.

Test-Retest Reliability of the Assessment of Fatty Liver Disease Using Low-Dose Computed Tomography in Cardiac Patients.

Non-alcoholic fatty liver disease (NAFLD) is a common disorder that is associated with the risk of cardiovascular diseases. Therefore, its prevalence is high in patients with coronary artery disease. In myocardial perfusion imaging (MPI), low-dose computed tomography (CT) scans are used for attenuation correction in separate stress and rest studies. Here, the test-retest reliability of CT-based quantification of NAFLD was evaluated using these two CT scans. The study population consisted of 261 patients (156 men and 105 women, age 66 ± 10 years). Quantification of liver fat content was based on the radiodensity of the liver in Hounsfield units as well as in relation to corresponding values of the spleen. NAFLD was observed in 47 subjects (18%). CT quantification has good test-retest reliability in assessing NAFLD, with concordance correlation coefficient (CCC) ranging from 0.512 to 0.923, intraclass correlation coefficient (ICC) ranging from 0.513 to 0.923, and coefficient of variation ranging from 3.1 to 7.0%. Regarding the liver to spleen ratio, CCC for non-NAFLD patients and NAFLD patients was 0.552 and 0.911, respectively. For non-NAFLD patients ICC was 0.553 and NAFLD patients it was 0.913. The coefficient of variation for non-NAFLD and NAFLD patients was 4.9% and 3.1%, respectively. Our results suggest that low-dose CT is a feasible and well repeatable method but amount of liver fat contributes to repeatability. In NAFLD patients CCC and ICC were high reflecting excellent reliability, whereas in non-NAFLD patients test-retest reliability was moderate. Assessment of liver fat content can be used as additional information in studies where a CT scan has been done for other medical reasons, such as for low-dose attenuation correction CT along with MPI.

Reference values for left ventricular systolic synchrony according to phase analysis of ECG-gated myocardial perfusion SPECT.

BACKGROUND: The aim of this study was to define reference values for left ventricular systolic synchrony and for the volume parameters of the left ventricle using myocardial perfusion SPECT-derived phase analysis method. METHODS: We evaluated data of 433 patients who underwent myocardial perfusion SPECT/CT during January 2012-February 2013 in Kuopio University Hospital. The final study population consisted of 52 patients (aged 42-84 years) who met the criteria: (1) no previously diagnosed cardiac disease, (2) normal ECG at rest, (3) no advanced coronary artery disease in CT and 4) normal myocardial perfusion in stress/rest myocardial perfusion SPECT/CT. The severity of mechanical dyssynchrony was assessed by phase analysis of gated myocardial SPECT at stress stage after pharmacological exercise and at rest using Quantitative Gated SPECT (QGS) software. Volume parameters of the left ventricle were also assessed. RESULTS: The phase histogram bandwidth at rest was 28.0 [63.7] degrees (median [95th percentile]). The standard deviation of phase histogram at rest was 7.8 [26.5] degrees. Entropy at the rest study was 54.0 [63.7] %. All left ventricular dyssynchrony parameters were statistically significantly higher at stress compared to rest. There were no statistically significant differences in dyssynchrony values between men and women. In volume parameters, reference values in male were expectedly higher than in female. Cardiac output did not differ significantly between genders. CONCLUSION: In subjects without signs of cardiac diseases, the left ventricular systolic function is well synchronized. Phase analysis measurement does not depend on gender, age, BMI or blood pressure, but the values of dyssynchrony parameters increase during pharmacological stress.

Characteristics and Outcomes of 79 Patients with an Insulinoma: A Nationwide Retrospective Study in Finland.

OBJECTIVE: Insulinomas are rare pancreatic tumours. Population-based data on their incidence, clinical picture, diagnosis, and treatment are almost nonexistent. The aim of this study was to clarify these aspects in a nationwide cohort of insulinoma patients diagnosed during three decades. DESIGN AND METHODS: Retrospective analysis on all adult patients diagnosed with insulinoma in Finland during 1980-2010. RESULTS: Seventy-nine patients were diagnosed with insulinoma over the research period. The median follow-up from diagnosis to last control visit was one (min 0, max 31) year. The incidence increased from 0.5/million/year in the 1980s to 0.9/million/year in the 2000s (p = 0.002). The median diagnostic delay was 13 months and did not change over the study period. The mean age at diagnosis was 52 (SD 16) years. The overall imaging sensitivity improved from 39% in the 1980s to 98% in the 2000s (p < 0.001). Seventy-one (90%) of the patients underwent surgery with a curative aim, two (3%) had palliative surgery, and 6 (8%) were inoperable. There were no significant differences in the types of surgical procedures between the 1980s, 1990s, and 2000s; tumour enucleations comprised 43% of the operations, distal pancreatic resections 45%, and pancreaticoduodenectomies 12%, over the whole study period. Of the patients who underwent surgery with a curative aim, 89% had a full recovery. Postoperative complications occurred in half of the patients, but postoperative mortality was rare. CONCLUSIONS: The incidence of insulinomas has increased during the past three decades. Despite the improved diagnostic options, diagnostic delay has remained unchanged. To shorten the delay, clinicians should be informed and alert to consider the possibility of hypoglycemia and insulinoma, when symptomatic attacks are investigated in different sectors of the healthcare system. Developing the surgical treatment is another major target, in order to lower the overall complication rate, without compromising the high cure rate of insulinomas.