Anca Florian

Subclinical cardiotoxicity detected by strain rate imaging up to 14 months after breast radiation therapy.

PURPOSE Strain rate imaging (SRI) is a new echocardiographic modality that enables accurate measurement of regional myocardial function. We investigated the role of SRI and troponin I (TnI) in the detection of subclinical radiation therapy (RT)-induced cardiotoxicity in breast cancer patients. METHODS AND MATERIALS This study prospectively included 75 women (51 left-sided and 24 right-sided) receiving adjuvant RT to the breast/chest wall and regional lymph nodes. Sequential echocardiographs with SRI were obtained before RT, immediately after RT, and 8 and 14 months after RT. TnI levels were measured on the first and last day of RT. RESULTS Mean heart and left ventricle (LV) doses were both 9 ± 4 Gy for the left-sided patients and 4 ± 4 Gy and 1 ± 0.4 Gy, respectively, for the right-sided patients. A decrease in strain was observed at all post-RT time points for left-sided patients (-17.5% ± 1.9% immediately after RT, -16.6% ± 1.4% at 8 months, and -17.7% ± 1.9% at 14 months vs -19.4% ± 2.4% before RT, P<.01) but not for right-sided patients. When we considered left-sided patients only, the highest mean dose was given to the anterior left ventricular (LV) wall (25 ± 14 Gy) and the lowest to the inferior LV wall (3 ± 3 Gy). Strain of the anterior wall was reduced after RT (-16.6% ± 2.3% immediately after RT, -16% ± 2.6% at 8 months, and -16.8% ± 3% at 14 months vs -19% ± 3.5% before RT, P<.05), whereas strain of the inferior wall showed no significant change. No changes were observed with conventional echocardiography. Furthermore, mean TnI levels for the left-sided patients were significantly elevated after RT compared with before RT, whereas TnI levels of the right-sided patients remained unaffected. CONCLUSIONS In contrast to conventional echocardiography, SRI detected a regional, subclinical decline in cardiac function up to 14 months after breast RT. It remains to be determined whether these changes are related to clinical outcome. In the meantime, we encourage the use of radiation techniques that minimize the exposure of the anterior LV wall in left-sided patients.

The diagnostic value of iron oxide nanoparticles for imaging of myocardial inflammation – quo vadis?

Cardiovascular magnetic resonance (CMR) is an integral part in the diagnostic work-up of cardiac inflammatory diseases. In this context, superparamagnetic iron oxide-based contrast agents can provide additional diagnostic information regarding the assessment of myocardial infarction and myocarditis. After intravenous administration, these nanoparticles are taken up by activated monocytes and macrophages, which predominantly accumulate in regions associated with inflammation as was successfully shown in recent preclinical studies. Furthermore, first clinical studies with a new iron oxide-complex that was clinically approved for the treatment of iron deficiency anaemia recently demonstrated a superior diagnostic value of iron oxide nanoparticles compared to gadolinium-based compounds for imaging of myocardial inflammation in patients with acute myocardial infarction. In this article, we outline the basic features of superparamagnetic iron oxide-based contrast agents and review recent studies using such nanoparticles for cardiac imaging in case of acute myocardial infarction as well as acute myocarditis. Moreover, we highlight the translational potential of these agents and possible research applications with regard to imaging and therapy.

Assessment of Early Post-Infarction Pericardial Injury by CMR

Early post-infarction pericardial injury is a marker of more extensive myocardial damage, but the diagnosis remains elusive because of a paucity of objective manifestations and the lack of universally accepted diagnostic criteria ([1,2][1]). In clinical practice, the diagnosis is based on presence

The emerging role of magnetic resonance imaging and multidetector computed tomography in the diagnosis of dilated cardiomyopathy

Magnetic resonance imaging and multidetector computed tomography are new imaging methods that have much to offer clinicians caring for patients with dilated cardiomyopathy. In this article we briefly describe the clinical, pathophysiological and histological aspects of dilated cardiomyopathy. Then we discuss in detail the use of both imaging methods for measurement of chamber size, global and regional function, for myocardial tissue characterisation, including myocardial viability assessment, and determination of arrhythmogenic substrate, and their emerging role in cardiac resynchronisation therapy.

Original ResearchElectrocardiographic Q-Wave “Remodeling” in Reperfused ST-Segment Elevation Myocardial Infarction: Validation Study With CMR

OBJECTIVES The aim of this study was to evaluate the evolution in Q-wave expression during the first 5 years after a primary, successfully reperfused ST-segment elevation myocardial infarction (MI), using cardiac magnetic resonance (CMR) for infarct location, and to depict changes in infarct size and left ventricular remodeling over time. BACKGROUND In the absence of QRS confounders, abnormal Q waves are usually diagnostic of myocardial necrosis. It is hypothesized that Q-wave regression after MI could be related to smaller infarct sizes. Late gadolinium enhancement accurately depicts MI of any age. METHODS Forty-six MI patients underwent electrocardiography and CMR at 1 week (baseline), 4 months, 1 year, and 5 years post-infarction. Conventional CMR parameters were analyzed, and infarct presence, location, and size were assessed using late gadolinium enhancement CMR. Infarct locations were anterior or nonanterior (inferior and/or lateral), using late gadolinium enhancement CMR as a reference. For each time point, patients were classified as having a diagnostic/nondiagnostic electrocardiogram (ECG) using the European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation consensus criteria for previous Q-wave infarct. RESULTS At baseline, 11 patients (23%) did not meet the criteria for Q-wave MI. Non-Q-wave infarcts were significantly smaller than Q-wave infarcts (p < 0.0001). All anterior Q-wave infarcts (n = 17) were correctly localized, whereas in 7 of 19 nonanterior Q-wave infarcts, the location or extent of the infarct was misjudged by electrocardiography. At 4-month/1-year follow-up, in 10 patients (3 anterior/7 nonanterior), the ECG became nondiagnostic. The ECG remained nondiagnostic at 5-year follow-up. A cutoff infarct size of 6.2% at 1 year yielded a sensitivity of 89% and a specificity of 74% to predict the presence or absence of Q waves. CONCLUSIONS The incidence of nondiagnostic ECGs for previous MI using the current European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation criteria is substantial and increases with time post-infarction from 23% immediately post-infarction to 44% at 5-year follow-up.

Electrocardiographic Q-wave "remodeling" in reperfused ST-segment elevation myocardial infarction: validation study with CMR.

OBJECTIVES The aim of this study was to evaluate the evolution in Q-wave expression during the first 5 years after a primary, successfully reperfused ST-segment elevation myocardial infarction (MI), using cardiac magnetic resonance (CMR) for infarct location, and to depict changes in infarct size and left ventricular remodeling over time. BACKGROUND In the absence of QRS confounders, abnormal Q waves are usually diagnostic of myocardial necrosis. It is hypothesized that Q-wave regression after MI could be related to smaller infarct sizes. Late gadolinium enhancement accurately depicts MI of any age. METHODS Forty-six MI patients underwent electrocardiography and CMR at 1 week (baseline), 4 months, 1 year, and 5 years post-infarction. Conventional CMR parameters were analyzed, and infarct presence, location, and size were assessed using late gadolinium enhancement CMR. Infarct locations were anterior or nonanterior (inferior and/or lateral), using late gadolinium enhancement CMR as a reference. For each time point, patients were classified as having a diagnostic/nondiagnostic electrocardiogram (ECG) using the European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation consensus criteria for previous Q-wave infarct. RESULTS At baseline, 11 patients (23%) did not meet the criteria for Q-wave MI. Non-Q-wave infarcts were significantly smaller than Q-wave infarcts (p < 0.0001). All anterior Q-wave infarcts (n = 17) were correctly localized, whereas in 7 of 19 nonanterior Q-wave infarcts, the location or extent of the infarct was misjudged by electrocardiography. At 4-month/1-year follow-up, in 10 patients (3 anterior/7 nonanterior), the ECG became nondiagnostic. The ECG remained nondiagnostic at 5-year follow-up. A cutoff infarct size of 6.2% at 1 year yielded a sensitivity of 89% and a specificity of 74% to predict the presence or absence of Q waves. CONCLUSIONS The incidence of nondiagnostic ECGs for previous MI using the current European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation criteria is substantial and increases with time post-infarction from 23% immediately post-infarction to 44% at 5-year follow-up.

Diagnostic value of global myocardial perfusion reserve assessment based on coronary sinus flow measurements using cardiovascular magnetic resonance in addition to myocardial stress perfusion imaging

Aims Myocardial perfusion reserve (MPR) is defined as the maximal possible increase in myocardial blood flow (MBF) above baseline conditions. Global MBF can be measured non-invasively by means of coronary sinus flow velocity encoded cine (VENC) cardiovascular magnetic resonance (CMR). We aimed to explore the relationship between global MBF/MPR and the extent and severity of coronary artery disease (CAD) in patients referred for CAD work-up by adenosine-stress CMR. Methods and results Fifty-eight patients with suspected obstructive CAD underwent both adenosine-stress CMR and invasive coronary angiography. In addition to standard cine- and late gadolinium enhancement (LGE)-imaging, first-pass myocardial perfusion imaging (MPI) and coronary sinus flow measurements (VENC) were performed at rest and during peak stress (after 140 µg/kg/min adenosine), respectively. Nineteen young patients with a very low CAD pre-test probability and normal adenosine-stress CMR formed the control group. Fifty-nine percent (n = 34) of the study group showed segmental, adenosine-induced myocardial perfusion defects compared to none of the control group (P < 0.001). Global MPR was lower in the study group compared to the control group: 2.3 (1.5-3.1) vs. 3.1 (2.0-4.3), P = 0.016. The SYNTAX score was higher in the study group patients with an impaired MPR (<2) compared to those with a preserved MPR (3.0 vs. 16.0, P = 0.01)-mainly due to higher prevalence of proximal epicardial stenoses (60% vs. 27%, P = 0.02) and multi-vessel disease (56% vs. 24%, P = 0.017). The diagnostic yield of stress CMR for the diagnosis of CAD (>50% stenosis) increased from 65to 88% when global MPR assessment was considered in addition to MPI (P = 0.025). Conclusions Global MBF and MPR values correlate with the anatomical extent and complexity of CAD and increase the diagnostic yield of non-invasive stress CMR in the work-up of CAD. CMR-based MBF and MPR measurements may play a future role in the evaluation of the total ischaemic burden-particularly in patients with multi-vessel disease.

Cause of Cardiac Disease in a Female Carrier of Duchenne Muscular Dystrophy Myocarditis Versus Genetic Cardiomyopathy Without Skeletal Myopathy

A 51-year–old woman experienced a respiratory tract infection with fever followed by persistent fatigue and muscle pain in her extremities for >2 months. Family history revealed a 30-year–old wheelchair-bound son with advanced myopathy suffering from Duchenne muscular dystrophy (DMD; deletion in the dystrophin gene). Blood analysis in the mother revealed an elevated total creatine kinase (CK) level of 479 U/L (normal, <190 U/L) with a normal creatine kinase-MB (CK-MB) level of 17 U/L (normal, <25 U/l). Additional workup of (skeletal) myopathy was composed of a calf muscle biopsy with normal histopathologic findings (Figure 1): in particular, there were no signs of structural abnormalities, inflammation, or dystrophin deficiency. Genetic analysis of blood cells revealed a heterozygous dystrophin gene mutation, and the female patient was identified as a–probably symptomatic–DMD carrier. Figure 1. Hematoxylin-eosin (HE) staining of a skeletal muscle biopsy sample taken from the female Duchenne muscular dystrophy carrier: regular-sized and -shaped myocytes can be seen. Inserted images show immunohistochemical dystrophin stainings (DYS) with 3 different dystrophin antibodies: there are no signs of dystrophin deficiency. In addition to muscle pain, she was also experiencing dyspnea on exertion and fatigue and, therefore, presented to our hospital. She was in an acceptable general condition, and her physical examination was unremarkable. Her resting ECG demonstrated sinus rhythm without any repolarization abnormalities. A cardiovascular magnetic resonance imaging (CMR) study was performed on a …

Atherothrombosis in 2 vascular territories in a young woman: importance of thrombophilia testing.

The diagnosis and management of complex and multiple inherited thrombophilias is still a challenge for the clinicians involved in this field, clinical events being the result of the interaction between genes, environmental or other acquired factors, and age. Moreover, various clinical manifestations as regards severity or type of event (venous or arterial thrombotic event, obstetrical complications) are cited in these patients. We present the case of a 20-year-old woman, with a 2-month history of third-generation contraceptive use and with recently diagnosed hypercholesterolemia, who presented ischemic events in 2 arterial territories: acute left lower limb ischemia and silent myocardial infarction. Screening tests for thrombophilia, including genetic testing, showed moderate hyperhomocysteinemia and 2 inherited thrombophilic defects. Invasive investigation of the coronary arteries showed the presence of advanced atherosclerotic disease. Management of this complex thrombophilia includes lifetime oral anticoagulation as well as a homocysteine-lowering strategy comprising lifestyle modification and group B (folic acid, B6, B12) vitamin supplementing.

Images in cardiovascular medicine: Primary cardiac leiomyosarcoma: when valvular disease becomes a vascular surgical emergency.

A 50-year-old previously healthy woman was referred to our department for suspected mitral valve endocarditis because of a 3-week history of fever, weight loss, and the echocardiographic discovery of a mitral valve mass. On admission, the patient was cachectic (body mass index of 18 kg/m2) and subfebrile (37.5°C) with dyspnea at rest, jugular vein distension, and tender liver enlargement. Her heart examination showed regular tachycardia (100 bpm), apical systolic murmur (3/6 degree), and diastolic rumble. The ECG showed sinus tachycardia (105 bpm) and signs of left atrial abnormality (wide, notched P wave measuring 140 ms; Figure 1). Chest x-ray revealed a cardiothoracic index of 0.6, with left atrial enlargement and interstitial edema (Figure 2). Figure 1. Twelve-lead ECG shows sinus rhythm, signs of left atrial abnormality (wide, notched P wave measuring 140 ms), and nonspecific ST-T changes. Figure 2. Posteroanterior chest x-ray reveals a cardiothoracic index of 0.6, signs of left atrial enlargement, and interstitial edema. Echocardiography showed an enlarged left atrium and a partially mobile mass on the mitral valve involving mainly the anterior leaflet and the anterolateral commissure (Figure 3A and 3B and Movies I and II in the online-only Data Supplement). …A 50-year-old previously healthy woman was referred to our department for suspected mitral valve endocarditis because of a 3-week history of fever, weight loss, and the echocardiographic discovery of a mitral valve mass. On admission, the patient was cachectic (body mass index of 18 kg/m2) and subfebrile (37.5°C) with dyspnea at rest, jugular vein distension, and tender liver enlargement. Her heart examination showed regular tachycardia (100 bpm), apical systolic murmur (3/6 degree), and diastolic rumble. The ECG showed sinus tachycardia (105 bpm) and signs of left atrial abnormality (wide, notched P wave measuring 140 ms; Figure 1). Chest x-ray revealed a cardiothoracic index of 0.6, with left atrial enlargement and interstitial edema (Figure 2). Figure 1. Twelve-lead ECG shows sinus rhythm, signs of left atrial abnormality (wide, notched P wave measuring 140 ms), and nonspecific ST-T changes. Figure 2. Posteroanterior chest x-ray reveals a cardiothoracic index of 0.6, signs of left atrial enlargement, and interstitial edema. Echocardiography showed an enlarged left atrium and a partially mobile mass on the mitral valve involving mainly the anterior leaflet and the anterolateral commissure (Figure 3A and 3B and Movies I and II in the online-only Data Supplement). …