Anterior STEMI associated with decreased strain in remote cardiac myocardium.

To assess (1) global longitudinal strain (GLS) by feature tracking cardiac magnetic resonance (CMR) in the sub-acute and chronic phases after ST-elevation infarction (STEMI) and compare to GLS in healthy controls, and (2) the evolution of GLS and regional longitudinal strain (RLS) over time, and their relationship to infarct location and size. Seventy-seven patients from the CHILL-MI-trial (NCT01379261) who underwent CMR 2-6 days and 6 months after STEMI and 27 healthy controls were included for comparison. Steady state free precession (SSFP) long-axis cine images were obtained for GLS and RLS, and late gadolinium enhancement (LGE) images were obtained for infarct size quantifications. GLS was impaired in the sub-acute (- 11.8 ± 3.0%) and chronic phases (- 14.3 ± 2.9%) compared to normal GLS in controls (- 18.4 ± 2.4%; p < 0.001 for both). GLS improved from sub-acute to chronic phase (p < 0.001). GLS was to some extent determined by infarct size (sub-acute: r2 = 0.2; chronic: r2 = 0.2, p < 0.001). RLS was impaired in all 6 wall-regions in LAD infarctions in both the sub-acute and chronic phase, while LCx and RCA infarctions had preserved RLS in remote myocardium at both time points. Global longitudinal strain is impaired sub-acutely after STEMI and improvement is seen in the chronic phase, although not reaching normal levels. Global longitudinal strain is only moderately determined by infarct size. Regional longitudinal strain is most impaired in the infarcted region, and LAD infarctions have effects on the whole heart. This could explain why LAD infarcts are more serious than the other culprit vessel infarctions and more often cause heart failure.

Evolution of left ventricular function among subjects with ST-elevation myocardial infarction after percutaneous coronary intervention.

BACKGROUND: Atrioventricular plane displacement (AVPD) reflects longitudinal left ventricular (LV) systolic function, and wall thickening (WT) regional radial LV function. The temporal evolution of these measures after STEMI with CMR has not been evaluated. We aimed to investigate how AVPD and WT are affected globally and regionally from the sub-acute to the chronic phase after ST-elevation myocardial infarction (STEMI). METHODS: Healthy volunteers without cardiovascular disease and medication (controls, n = 20) and patients from the CHILL-MI study ( NCT01379261 ) prospectively underwent magnetic resonance imaging (MRI) 2-6 days and 6 months after STEMI (n = 77). CHILL-MI randomized STEMI-patients to cooling therapy initiated before reperfusion or standard of care. AVPD was measured at six points in three long axis cine images and wall thickening in short axis cine images. Infarction was quantified using late gadolinium enhancement (LGE) and used to define infarct and remote segments. RESULTS: There were no difference in AVPD either at acute or chronic phase (p = 0.90 and p = 0.40) or WT (p = 0.85 and p = 0.99) between patients randomized to cooling therapy and standard of care. Therefore, the results are presented for the pooled cohort. Global AVPD was decreased in both the sub-acute (12 ± 2 mm, p < 0.001) and the chronic phase (13 ± 2 mm, p < 0.001) compared to controls (15 ± 2 mm) with a partial recovery of AVPD (p < 0.001) in the chronic phase. Patients with left anterior descending (LAD) and right coronary artery (RCA) infarcts had decreased AVPD in the chronic phase in both infarcted and remote segments. Mean WT was decreased in patients with LAD infarction both in the sub-acute and the chronic phase in both infarcted and remote segments. The decrease in WT in patients with RCA and left circumflex (LCx) infarcts was more affected in the infarcted segments, especially in the chronic phase. CONCLUSION: AVPD was a global rather than regional marker of cardiac function in this STEMI study and this may explain the prognostic importance of local measurements of mitral annular plane systolic excursion (MAPSE). The decrease in WT in remote myocardium even in the chronic phase needs to be taken into consideration when combining functional measurements with infarct quantification for diagnosis of post-ischemic stunning and hibernation.

[Swedish emergency physicians can safely sedate patients with propofol prior to cardioversion]. / Akutläkardriven propofolsedering är säker vid elkonvertering.

Emergency Medicine became a full-fledged speciality in Sweden in 2015. This prospective study analyzed the safety and implementation of Emergency Physician-administered propofol to sedate patients with hemodynamically stable atrial fibrillation prior to cardioversion. During the first 1.5 years, 321 sedations were carried out at Lund's Emergency Department by Emergency Physicians or senior residents. In two cases, the oxygen saturation dipped below 90% before responding to simple measures. In 12 cases, the systolic blood pressure dipped below 90 mmHg, and in two cases patients were administered a push-dose pressor. No patient required hospitalization due to sedation-induced complications. The majority of eligible specialists and senior residents voluntarily participated in an Emergency Physician-driven certification process. This study demonstrates the safety and feasibility of a locally implemented process for Emergency Physician-driven procedural sedation.

Longitudinal left ventricular function is globally depressed within a week of STEMI.

Sixty percent of stroke volume (SV) is generated by atrioventricular plane displacement (AVPD) in a healthy left ventricle (LV). The aims were to determine the effect of ST-elevation myocardial infarction (STEMI) on AVPD and contribution of AVPD to SV and to study the relationship between AVPD and infarct size (IS) and location. Patients from CHILL-MI and MITOCARE studies with cardiovascular magnetic resonance within a week of STEMI (n = 177, 59 ± 11 years) and healthy controls (n = 20, 62 ± 11 years) were included. Left ventricular volumes were quantified in short-axis images. AVPD was measured in six locations in long-axis images. Longitudinal contribution to SV was calculated as AVPD multiplied by the short-axis epicardial area. Patients (IS 17 ± 10% of LV) had decreased ejection fraction (48 ± 8%) compared to controls (60 ± 5%, P<0·001). Global AVPD was decreased in patients (11 ± 2 mm versus 15 ± 2 mm in controls, P<0·001) and this held true for both infarcted and remote segments. AVPD contribution to SV was lower in patients (58 ± 9%) than in controls (64 ± 8%) (P<0·001). There was a weak negative correlation between IS and AVPD (r2 =0·06) but no differences in global AVPD linked to infarct location. Decrease in global and regional AVPD occur even in remote myocardium within 1 week of STEMI. Global AVPD decrease is independent of MI location, and MI size has only minor effect. Longitudinal pumping is slightly lower compared to controls but remains to be the main component to SV even after STEMI. These results highlight the difficulty in determining infarct location and size from longitudinal measures of LV function.

Longitudinal shortening remains the principal component of left ventricular pumping in patients with chronic myocardial infarction even when the absolute atrioventricular plane displacement is decreased.

BACKGROUND: The majority (60%) of left ventricular (LV) stroke volume (SV) is generated by longitudinal shortening causing apical atrioventricular plane displacement (AVPD) in systole. The remaining SV is caused by radial inward motion of the epicardium both in the septal and the lateral wall. We aimed to determine if these longitudinal, septal and lateral contributions to LVSV are changed in patients with chronic myocardial infarction (MI). METHODS: Patients with a chronic (>3 months) ST-elevation MI in the left anterior descending (LAD, n = 20) or right coronary artery (RCA, n = 16) and healthy controls (n = 20) were examined with cardiovascular magnetic resonance (CMR). AVPD was quantified in long axis cine CMR images and LV volumes and dimensions in short axis cine images. RESULTS: AVPD was decreased both in patients with LAD-MI (11 ± 1 mm, p < 0.001) and RCA-MI (13 ± 1 mm, p < 0.05) compared to controls (15 ± 0 mm). However, the longitudinal contribution to SV was unchanged for both LAD-MI (58 ± 3%, p = 0.08) and RCA-MI (59 ± 3%, p = 0.09) compared to controls (64 ± 2%). The preserved longitudinal contribution despite decreased absolute AVPD was a results of increased epicardial dimensions (p < 0.01 for LAD-MI and p = 0.06 for RCA-MI). In LAD-MI the septal contribution to LVSV was decreased (5 ± 1%) compared to both controls (10 ± 1%, p < 0.01) and patients with RCA-MIs (10 ± 1%, p < 0.01). The lateral contribution was increased in LAD-MI patients (44 ± 3%) compared to both RCA-MI (35 ± 2%, p < 0.05) and controls (29 ± 2%, p < 0.001). CONCLUSION: Longitudinal shortening remains the principal component of left ventricular pumping in patients with chronic MI even when the absolute AVPD is decreased.

Time-resolved tracking of the atrioventricular plane displacement in Cardiovascular Magnetic Resonance (CMR) images.

BACKGROUND: Atrioventricular plane displacement (AVPD) is an indicator for systolic and diastolic function and accounts for 60% of the left ventricular, and 80% of the right ventricular stroke volume. AVPD is commonly measured clinically in echocardiography as mitral and tricuspid annular plane systolic excursion (MAPSE and TAPSE), but has not been applied widely in cardiovascular magnetic resonance (CMR). To date, there is no robust automatic algorithm available that allows the AVPD to be measured clinically in CMR with input in a single timeframe. This study aimed to develop, validate and provide a method that automatically tracks the left and right ventricular AVPD in CMR images, which can be used in the clinical setting or in applied cardiovascular research in multi-center studies. METHODS: The proposed algorithm is based on template tracking by normalized cross-correlation combined with a priori information by principal component analysis. The AVPD in each timeframe is calculated for the left and right ventricle separately using CMR long-axis cine images of the 2, 3, and 4-chamber views. The algorithm was developed using a training set (n = 40), and validated in a test set (n = 113) of healthy subjects, athletes, and patients after ST-elevation myocardial infarction from 10 centers. Validation was done using manual measurements in end diastole and end systole as reference standard. Additionally, AVPD, peak emptying velocity, peak filling velocity, and atrial contraction was validated in 20 subjects, where time-resolved manual measurements were used as reference standard. Inter-observer variability was analyzed in 20 subjects. RESULTS: In end systole, the difference between the algorithm and the reference standard in the left ventricle was (mean ± SD) -0.6 ± 1.9 mm (R = 0.79), and -0.8 ± 2.1 mm (R = 0.88) in the right ventricle. Inter-observer variability in end systole was -0.6 ± 0.7 mm (R = 0.95), and -0.5 ± 1.4 mm (R = 0.95) for the left and right ventricle, respectively. Validation of peak emptying velocity, peak filling velocity, and atrial contraction yielded lower accuracy than the displacement measures. CONCLUSIONS: The proposed algorithm show good agreement and low bias with the reference standard, and with an agreement in parity with inter-observer variability. Thus, it can be used as an automatic method of tracking and measuring AVPD in CMR.

Regional wall function before and after acute myocardial infarction; an experimental study in pigs.

BACKGROUND: Left ventricular function is altered during and after AMI. Regional function can be determined by cardiac magnetic resonance (CMR) wall thickening, and velocity encoded (VE) strain analysis. The aims of this study were to investigate how regional myocardial wall function, assessed by CMR VE-strain and regional wall thickening, changes after acute myocardial infarction, and to determine if we could differentiate between ischemic, adjacent and remote segments of the left ventricle. METHODS: Ten pigs underwent baseline CMR study for assessment of wall thickening and VE-strain. Ischemia was then induced for 40-minutes by intracoronary balloon inflation in the left anterior descending coronary artery. During occlusion, (99m)Tc tetrofosmin was administered intravenously and myocardial perfusion SPECT (MPS) was performed for determination of the ischemic area, followed by a second CMR study. Based on ischemia seen on MPS, the 17 AHA segments of the left ventricle was divided into 3 different categories (ischemic, adjacent and remote). Regional wall function measured by wall thickening and VE-strain analysis was determined before and after ischemia. RESULTS: Mean wall thickening decreased significantly in the ischemic (from 2.7 mm to 0.65 mm, p < 0.001) and adjacent segments (from 2.4 to 1.5 mm p < 0.001). In remote segments, wall thickening increased significantly (from 2.4 mm to 2.8 mm, p < 0.01). In ischemic and adjacent segments, both radial and longitudinal strain was significantly decreased after ischemia (p < 0.001). In remote segments there was a significant increase in radial strain (p = 0.002) while there was no difference in longitudinal strain (p = 0.69). ROC analysis was performed to determine thresholds distinguishing between the different regions. Sensitivity for determining ischemic segments ranged from 70-80%, and specificity from 72%-77%. There was a 9% increase in left ventricular mass after ischemia. CONCLUSION: Differentiation thresholds for wall thickening and VE-strain could be established to distinguish between ischemic, adjacent and remote segments but will, have limited applicability due to low sensitivity and specificity. There is a slight increase in radial strain in remote segments after ischemia. Edema was present mainly in the ischemic region but also in the combined adjacent and remote segments.

The 24-lead ECG display for enhanced recognition of STEMI-equivalent patterns in the 12-lead ECG.

In a patient with chest pain and suspected acute coronary syndrome, the electrocardiogram (ECG) is the only readily available diagnostic tool. It is important to maximize its usefulness to detect acute myocardial ischemia that may evolve to myocardial infarction unless the patient is treated expediently with reperfusion therapy. Since diagnostic guidelines have usually included only ST-elevation myocardial infarction (STEMI) as the entity that should be diagnosed and treated urgently, a patient with coronary occlusion represented on ECG as ST depression is likely not to be considered a candidate for receiving immediate coronary angiography and coronary intervention. ECG criteria for STEMI detection require that ST elevation meet predetermined millivolt thresholds and appear in at least two spatially contiguous ECG leads. The typical ECG reader recognizes only three contiguous pairs: aVL and I; II and aVF; aVF and III. However, viewing the "orderly sequenced" 12-lead ECG display, two more contiguous pairs become obvious in the frontal plane: +I and -aVR; -aVR and +II. The 24-lead ECG is a display of the standard 12-lead ECG as both the classical positive leads and their negative (inverted) counterparts. Leads +V1, +V2, +V3, +V4, +V5, and +V6 and their inverted counterparts are used to generate a "clock-face display" for the transverse plane. Similarly, +aVL, +I, -aVR, +II, +aVF, +III in the frontal plane and their inverted counterparts are used to generate a clock-face display for the frontal plane. Optimum results, 78% sensitivity and 93% specificity, were obtained using the following 19 ECG leads: frontal plane: +aVR, -III, +aVL, +I, -aVR, +II, +aVF, +III, -aVL; transverse plane: +V1, +V2, +V3, +V4, +V5, +V6, -V1, -V2, -V3.