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Response to cardiac resynchronization therapy (CRT) is hampered by the extent and location of left ventricular (LV) scar tissue. It is commonly advised to avoid scar tissue while placing the LV lead. However, whether individual patients benefit from this strategy remains unclear. Thirty-two CRT candidates with ischemic cardiomyopathy were enrolled from 2 successive clinical trials (TBS and E-pot study). Magnetic resonance imaging with late contrast enhancement was performed to assess location, degree and transmurality of LV scar tissue. Patients underwent invasive pressure-volume loop measurements to assess acute LV pump function changes during pacing at posterolateral (PL) and anterolateral LV sites. In the study population (26 [81%] men, ejection fraction [EF] 22% ± 8%, QRS 149 ± 20 milliseconds), baseline mean stroke work (SW) and dP/dtmax were 4.4 ± 2.2 L∙mmHg and 849 ± 212 mmHg/s, respectively. The extent of scar tissue was inversely related to the acute increase in SW during pacing (R = −0.53, P = .002). Stimulating PL scar tissue resulted in deterioration of pump function (∆SW −17% ± 17%, P = .018), whereas pacing PL viable tissue led to an increase in pump function (∆SW +62% ± 51%, P < .001). Switching from pacing at the location of scar tissue, irrespective of the scar location, to viable tissue showed a significant increase in SW (−8% ± 20% vs +20 ± 40, P = .004). The extent of LV scar tissue is inversely related to acute pump function improvement during CRT. Pacing at the location of (transmural) scar tissue at any site of the LV will generally deteriorate LV pump function. Placing the LV lead over viable myocardium significantly improves pump function as compared with pacing at the location of scar tissue in patients with ischemic cardiomyopathy.

A varying degree of interstitial and perivascular fibrosis is a common finding in idiopathic dilated cardiomyopathy (DCM). The perfusable tissue index (PTI), obtained with PET, is a noninvasive tool for assessing myocardial fibrosis on a regional level. Measurements of the PTI in DCM, however, have not been performed yet. This study was undertaken to test the hypothesis that the PTI is reduced in patients with DCM. Fifteen patients with an advanced stage of DCM (New York Heart Association class III or IV and left ventricular ejection fraction [LVEF] < 35%) and 11 healthy control subjects were studied. PET was performed using H(2)(15)O and C(15)O to obtain the perfusable tissue fraction (PTF) and the anatomic tissue fraction (ATF), respectively. The PTI (=PTF/ATF) was reduced in DCM compared with control subjects (0.91 +/- 0.12 vs. 1.12 +/- 0.10; P < 0.01). Heterogeneity of the PTI, expressed as the coefficient of variation, was increased in DCM versus that of healthy control subjects (0.18 +/- 0.07 vs. 0.13 +/- 0.06; P < 0.05). There was no correlation between the PTI and echocardiographically derived LVEF in both groups. The PTI was reduced in patients with an advanced stage of DCM. Interstitial and perivascular fibrosis may be responsible for this reduction. Furthermore, the degree of the PTI reduction was variable in DCM patients, both on a regional level and between patients. Noninvasive assessment of fibrosis with the PTI offers the opportunity to evaluate the effects of fibrosis on regional myocardial function, correlate fibrosis with prognosis, and monitor pharmaceutical intervention.

Although resynchronisation therapy (CRT) is a promising addition to heart failure therapy, a substantial number of patients do not respond to CRT. As FDG PET has routinely been used for prediction of improvement after revascularisation in ischaemic cardiomyopathy, it was hypothesised that there is also a relationship between the extent of viable tissue and improvement as a result of CRT. Thirty-nine patients with ischaemic cardiomyopathy (ejection fraction 27 +/- 9%) and a wide QRS complex underwent temporary pacing to determine the optimal pacing combination, i.e. that with the highest increase in cardiac index (CI) compared with baseline (measured by Doppler echocardiography). All patients also underwent FDG PET imaging. In 19 patients, CI measurements were repeated 10-12 weeks after permanent biventricular pacemaker implantation. Echocardiography (13-segment model) showed a mean of 9.8 +/- 1.6 dyssynergic segments, with preserved FDG uptake in 4.1 +/- 2.4 segments. CI improvement at the optimal pacing site was 20 +/- 9%. There was a linear relationship between the extent of viable tissue and CI improvement during pacing (p < 0.001). Using a cut-off value of more than three viable segments (ROC analysis), FDG PET had a sensitivity of 72% and a specificity of 71% for detection of the presence of haemodynamic improvement (i.e. a CI improvement >15%). The relation between CI improvement and viable tissue was similar at follow-up. A correlation was found between the extent of viable tissue and the haemodynamic response to CRT in patients with ischaemic cardiomyopathy, suggesting that FDG PET imaging may be useful to discriminate between responders and non-responders to CRT.

The effects of different breath-holding positions during electrocardiographic (ECG) recording on the QRS complex are unknown. In 73 subjects, ECG recordings were made in 3 different breath-holding positions: normal expiration (rest), maximum inspiration, and maximum expiration. QRS wave excursions and changes in the frontal electrical heart axis were analyzed. The mean effect of respiration in most leads was small (≥1 mm only in the S wave in V 4 and in the R wave in V 5), but the degree of interindividual variability was often substantial, with standard deviations of ≥1.5 mm in multiple leads. The effect of different extreme breath-holding positions on the QRS complex is on average small but may be substantial in individuals. Lack of standardization of breathing instructions during recording of the ECG may result in differences in application of amplitude criteria and poorer reproducibility.

Reports the case of a 17-year-old male who collapsed suddenly as the result of myocardial ischemia which may or may not have been caused by myocardial bridging. Source: National Library of New Zealand Te Puna Matauranga o Aotearoa, licensed by the Department of Internal Affairs for re-use under the Creative Commons Attribution 3.0 New Zealand Licence.

Analysis of coronary flow velocity pattern has been used to assess microvascular function post acute myocardial infarction (AMI). This study sought to analyze whether the flow level has an impact on parameters of coronary flow velocity pattern. Parameters of coronary flow velocity pattern were determined at baseline and during increased flow due to maximal hyperemia induced by adenosine in 25 patients after PTCA for first AMI using Doppler flow wires. Patients were divided into those with depressed (global wall motion index (GWMI) > or = 1.5; n = 14) and those with preserved (GWMI < 1.5; n = 11) left ventricular (LV) function at 4 weeks. Coronary flow velocity pattern at rest was different between patients with depressed and patients with preserved LV function at follow-up. A difference in flow pattern between the groups remained at increased flow level. However, increase of flow altered parameters of flow pattern. Diastolic deceleration rate (DSR) increased for patients with preserved LV function (53.7+/-25.6 at baseline vs. 67.0+/-29.8 cm/s2 with adenosine) and depressed LV function (95.3+/-58.6 vs. 110.7+/-61.4 cm/s2, respectively, p = 0.0012). Induction of hyperemia resulted also in increased systolic and diastolic peak flow velocity and diastolic deceleration time (DDT). Higher flow had no impact on early systolic retrograde flow, systolic flow duration and diastolic-systolic velocity ratio (DSVR). The coronary flow velocity pattern allows prediction of LV function at 4 weeks after AMI. However, it should be considered that some parameters of the flow velocity pattern are affected by the coronary flow level.