Hedvig Andersson

Takotsubo cardiomyopathy, a two-stage recovery of left ventricular systolic and diastolic function as determined by cardiac magnetic resonance imaging

AIMS Takotsubo cardiomyopathy (TTC) is an entity mimicking acute myocardial infarction, characterized by transient severe systolic heart failure. Echocardiographic studies suggest that diastolic dysfunction is present in TTC at presentation; however, no reports exist regarding the time course of left ventricular (LV) recovery. This study describes the recovery of LV systolic and diastolic function in TTC. We hypothesized that, in TTC, there is diastolic dysfunction at admission, and that recovery is delayed compared with systolic function. METHODS AND RESULTS We enrolled (consecutively 2010-12) 16 patients (mean age 66, range 39-84 years) diagnosed with TTC and 20 healthy matched controls. We performed cardiac magnetic resonance imaging (CMR) at admission, pre-discharge, and 3-month follow-up. Diastolic function was assessed by LV peak filling rate (LVPFR) and left atrial (LA) emptying volumes. At admission, LV ejection fraction was low, increased at pre-discharge (37 ± 6 vs. 58 ± 6%, P < 0.001), and normalized at follow-up (to 65 ± 5%, P = 0.01). LVPFR did not increase during hospitalization (80 ± 3 vs. 89 ± 4 mL/s/m(2), P = 0.21), but was normalized at follow-up (to 206 ± 19, P < 0.001; controls, 214 ± 13, P = 0.23). During hospitalization, LA passive emptying volume remained low (6 ± 2 vs. 8 ± 3 mL/m(2), P = 0.05) and LA active emptying volume remained high (17 ± 3 vs. 16 ± 3 mL/m(2), P = 0.71), whereas LA conduit volume increased (7 ± 3 vs. 23 ± 4 mL/m(2), P < 0.001). T2-weighted imaging demonstrated non-coronary distributed apical oedema without contrast enhancement. CONCLUSION Patients with TTC undergo fast systolic recovery. However, at discharge, profound diastolic dysfunction is demonstrated by CMR. At follow-up, both LV systolic and diastolic function is normalized in patients with recovered TTC.

Basal hyperaemia is the primary abnormality of perfusion in Takotsubo cardiomyopathy: a quantitative cardiac perfusion positron emission tomography study

AIMS Takotsubo cardiomyopathy (TTC) is characterized by acute completely reversible regional left ventricle (LV) akinesia and decreased tracer uptake in the akinetic region on semi-quantitative perfusion imaging. The latter may be due to normoperfusion of the akinetic mid/apical area and basal hyperperfusion. Our aim was to examine abnormalities of perfusion in TTC, and we hypothesized that basal hyperperfusion is the primary perfusion abnormality in the acute state. METHOD AND RESULTS Twenty-five patients were diagnosed with TTC due to (i) acute onset of symptoms, (ii) typical apical ballooning, (iii) absence of significant coronary disease, and (iv) complete remission on 4-month follow-up. The patients underwent coronary angiography (CAG), echocardiography, cardiac magnetic resonance imaging (CMR), and (13)NH3/(82)Rb positron emission tomography (PET) in the acute state and-except CAG-on follow-up. Patients initially had severe heart failure, mid/apical oedema but no infarction, and a rise in cardiac biomarkers. On initial perfusion PET imaging, eight patients appeared to have normal, whereas 17 patients had impaired LV perfusion. In the latter, flow in the basal region was increased in the acute state (1.5 ± 0.1 vs. 1.2 ± 0.1 mL/g/minRPP-corrected, P < 0.01), whereas midventricular (1.7 ± 0.1 vs. 1.6 ± 0.1 mL/g/minRPP-corrected, P = 0.21) and apical (1.4 ± 0.1 vs. 1.5 ± 0.1 mL/g/minRPP-corrected, P = 0.36) flow was unchanged between acute and follow-up, and within normal range. CONCLUSION Our results suggest an abnormal LV perfusion distribution in the acute state of TTC with basal hyperperfusion and a normoperfused akinetic region. The proportion of patients without visualized perfusion abnormalities in the acute state may represent a subgroup with fast remission.

Takotsubo-cardiomyopathy: A case of extremely fast recovery described by multimodality cardiac imaging

A 67-year-old male was admitted on the suspicionof STEMI due to chest pain after strenuous work, lateralST-elevation on ECG and troponin T 523 ng/L (ref.\50 ng/L). He had hypertension, hypercholesterolaemiaand was an ex-smoker but was otherwise healthy. Acutecoronary angiography showed no culprit lesion butapical ballooning on ventriculography (Figure 1A).Several image modalities were performed as part of aresearch protocol:Cardiac SPECT during resting conditions 15 hours afteradmission (Figure 1B) showed a relative perfusionreductionoftheapexandmidventricularpart,extent40%.Cardiac MRI 22 h after admission (Figure 1C) showedapical ballooning and LVEF 40% (ref. 56%-78%) andbasal hypercontractility, but no sign of infarction.Echocardiography 35 h after admission (Figure 1D)showed an akinetic apex and LVEF 50%.A second cardiac MRI 48 hours after admission(Fig. 1E) showed normalized LVEF 70%, but persis-tent apical hypokinesia and edema.N

Long-term survival and causes of death in patients with ST-elevation acute coronary syndrome without obstructive coronary artery disease

Aims We aimed to study survival and causes of death in patients with ST-elevation acute coronary syndrome (STE-ACS) with and without obstructive coronary artery disease (CAD). Methods and results We included 4793 consecutive patients with STE-ACS triaged for acute coronary angiography at a large cardiac invasive centre (2009-2014). Of these, 88% had obstructive CAD (stenosis ≥50%), 6% had non-obstructive CAD (stenosis 1-49%), and 5% had normal coronary arteries. Patients without obstructive CAD were younger and more often female with fewer cardiovascular risk factors. Median follow-up time was 2.6 years. Compared with patients with obstructive CAD, the short-term hazard of death (≤30 days) was lower in both patients with non-obstructive CAD [hazard ratio (HR) 0.49, 95% confidence interval (CI) 0.27-0.89, P = 0.018] and normal coronary arteries (HR 0.31, 95% CI 0.11-0.83, P = 0.021). In contrast, the long-term hazard of death (>30 days) was similar in patients with non-obstructive CAD (HR 1.15, 95% CI 0.77-1.72, P = 0.487) and higher in patients with normal coronary arteries (HR 2.44, 95% CI 1.58-3.76, P < 0.001), regardless of troponin levels. Causes of death were cardiovascular in 70% of patients with obstructive CAD, 38% with non-obstructive CAD, and 32% with normal coronary arteries. Finally, patients without obstructive CAD had lower survival compared with an age and sex matched general population. Conclusions STE-ACS patients without obstructive CAD had a long-term risk of death similar to or higher than patients with obstructive CAD. Causes of death were less often cardiovascular. This suggests that STE-ACS patients without obstructive CAD warrant medical attention and close follow-up.

Prevalence of acute cardiac disorders in patients with suspected ST-segment elevation myocardial infarction and non-significant coronary artery disease

BACKGROUND AND PURPOSE We aimed to study the prevalence of acute cardiac disorders in patients with suspected ST-segment elevation myocardial infarction (STEMI) and non-significant coronary artery disease (CAD). METHODS From January to October 2012 we consecutively included patients admitted with suspected STEMI and non-significant CAD (coronary artery stenosis diameter <50%). Patients were diagnosed with acute cardiac disorder in the presence of elevated cardiac biomarkers (troponin T >50ng/l or creatine kinase MB >4μg/l) or dynamic ECG changes (ST-segment changes or T-wave inversion). RESULTS Of the 871 patients admitted with suspected STEMI, 11% (n=95) had non-significant CAD. Of these, 67% (n=64) had elevated cardiac biomarkers or dynamic ECG changes and were accordingly diagnosed with acute cardiac disorders. In the remaining 33% (n=31) of patients, cardiac biomarkers were normal and ECG changes remained stationary. CONCLUSIONS Acute cardiac disorders were diagnosed in two thirds of patients with suspected STEMI and non-significant CAD.

Prognosis and high-risk complication identification in unselected patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Abstract Aims: The aim of this study was to evaluate treatment with primary percutaneous coronary intervention (PCI) in unselected patients with ST-segment elevation myocardial infarction (STEMI). Methods: We registered complication and mortality rates in all patients with STEMI admitted for primary PCI at a high-volume center over a two-year period (2004 to 2006). Results: We included 1022 consecutive patients (mean age 64 years; 69% men). In-hospital and one-year mortality were 8% and 12%, respectively. Cardiac arrest, cardiogenic shock, left ventricular ejection fraction ≤40% and atrioventricular block significantly predicted increased one-year mortality in univariate analysis (P < 0.001 for all) and were considered high-risk complications. 65% of patients had no high-risk complications. One-year mortality for patients without high-risk complications was 4% compared with 28% for those with high-risk complications (P < 0.001). Conclusion: Unselected patients with STEMI treated with primary PCI have mortality rates corresponding to those reported in randomized clinical studies including transport of patients. Mortality is strongly related to high-risk complications developed during admission. Thus, patients with high-risk complications should receive special attention. The majority of patients (65%) without high-risk complications have an excellent short- and long-term prognosis following primary PCI.

The effect of TIcagrelor administered through a nasogastric tube to COMAtose patients undergoing acute percutaneous coronary intervention: the TICOMA study

AIMS Patients in a coma after cardiac arrest may have adversely affected drug absorption and metabolism. This study, the first of its kind, aimed to investigate the early pharmacokinetic and pharmacodynamic effects of ticagrelor administered through a nasogastric tube (NGT) to patients resuscitated after an out of hospital cardiac arrest (OHCA) and undergoing primary percutaneous coronary intervention (pPCI). METHODS AND RESULTS Blood samples were drawn at baseline and at two, four, six, eight, 12, and 24 hours and then daily for up to five days after administration of a 180 mg ticagrelor loading dose (LD), followed by 90 mg twice daily in 44 patients. The primary endpoint was the occurrence of high platelet reactivity (HPR) 12 hours after the LD. Assessment by VerifyNow (VFN) showed 96 (15.25-140.5) platelet reactivity units (PRU), and five (12%) patients exhibited HPR. Multiplate analysis showed 19 (12-29) units (U) at twelve hours, and three patients (7%) had HPR. Ticagrelor and its main metabolite AR-C124910XX concentrations were 85.2 (37.2-178.5) and 18.3 (6.4-52.4) ng/mL. Median times to sufficient platelet inhibition below the HPR limit were 3 (2-6) hours (VFN) and 4 (2-8) hours (Multiplate). CONCLUSIONS Ticagrelor, administered as crushed tablets through a nasogastric tube, leads to sufficient platelet inhibition after 12 hours, and in many cases earlier, in the vast majority of patients undergoing pPCI and subsequent intensive care management after an OHCA.

Diagnostic accuracy of pace spikes in the electrocardiogram to diagnose paced rhythm.

OBJECTIVE To determine how often cardiac resynchronization therapy (CRT) pacing systems generate visible pace spikes in the electrocardiogram (ECG). METHODS In 46 patients treated with CRT pacing systems, we recorded ECGs during intrinsic rhythm, atrial pacing and ventricular pacing. ECGs were analysed for atrial and ventricular pace spikes by two experienced ECG readers blinded to the pacing therapy and to the study purpose. RESULTS Atrial pacing generated visible pace spikes in less than 70% of the ECGs, whereas ventricular pacing generated visible pace spikes in about 90% of ECGs. The sensitivity of manual ECG interpretation for pace spikes was low for atrial pacing (Reader 1: 0.62 [95% confidence interval (CI) 0.50-0.74]; Reader 2: 0.65 [95% CI 0.53-0.77]) and moderate for ventricular pacing (Reader 1: 0.88 [95% CI 0.81-0.93]; Reader 2: 0.93 [95% CI 0.87-0.97]). CONCLUSIONS In patients with CRT pacing systems, the absence of visible pace spikes in the ECG does not rule out paced rhythm.

Automatic electrocardiographic algorithm for assessing severity of ischemia in ST-segment elevation myocardial infarction

BACKGROUND Terminal QRS distortion on the electrocardiogram (ECG) is a sign of severe ischemia in patients with STEMI and can be quantified by the Sclarovsky-Birnbaum Severity of Ischemia. Due to score complexity, it has not been applied in clinical practice. Automatic scoring of digitally recorded ECGs could facilitate clinical application. We aimed to develop an automatic algorithm for the severity of ischemia. METHODS Development set: 50 STEMI ECGs were manually (Manual-score) and automatically (Auto-score) scored by our designed algorithm. The agreement between Manual- and Auto-score was assessed by kappa statistics. Test set: ECGs from 199 STEMI patients were assigned a severity grade (severe or non-severe ischemia) by the Auto-score. Infarct size estimated by median peak Troponin T (TnT) and Creatinine Kinase Myocardial Band (CKMB) was tested between the groups. RESULTS The agreement between Manual- and Auto-score was 0.83 ((95% CI 0.55-1.00), p < 0.0001), sensitivity 75% and specificity 100%, PPV 100% and NPV 94.6%. In the test set 152 (76%) patients were male, mean age 61 ± 12 years. The Auto-score designated severe ischemia in 42 (21%) and non-severe ischemia in 157 (79%) patients. Patients with ECG signs of severe vs. non-severe ischemia had significantly higher levels of biomarkers of infarct size. In multiple linear regression, ECG sign of severe ischemia was an independent predictor for higher TnT and CKMB levels. CONCLUSION The automatic ECG algorithm for severity of ischemia in STEMI performs adequately for clinical use. Severe ischemia obtained by the Auto-score was associated with biomarker estimated larger infarct size.

A Review of Automated Methods for Detection of Myocardial Ischemia and Infarction Using Electrocardiogram and Electronic Health Records

There is a growing body of research focusing on automatic detection of ischemia and myocardial infarction (MI) using computer algorithms. In clinical settings, ischemia and MI are diagnosed using electrocardiogram (ECG) recordings as well as medical context including patient symptoms, medical history, and risk factors—information that is often stored in the electronic health records. The ECG signal is inspected to identify changes in the morphology such as ST-segment deviation and T-wave changes. Some of the proposed methods compute similar features automatically while others use nonconventional features such as wavelet coefficients. This review provides an overview of the methods that have been proposed in this area, focusing on their historical evolution, the publicly available datasets that they have used to evaluate their performance, and the details of their algorithms for ECG and EHR analysis. The validation strategies that have been used to evaluate the performance of the proposed methods are also presented. Finally, the paper provides recommendations for future research to address the shortcomings of the currently existing methods and practical considerations to make the proposed technical solutions applicable in clinical practice.