Myocardial Dyskinesia Research Articles

To what extent are perfusion defects seen by myocardial perfusion SPECT in patients with left bundle branch block related to myocardial infarction, ECG characteristics, and myocardial wall motion?

IntroductionWe investigated if uptake pattern on myocardial perfusion SPECT (MPS) in patients with left bundle branch block (LBBB) is related to myocardial fibrosis, myocardial wall motion, and electrocardiography (ECG) characteristics. MethodsTwenty-three patients (9 women) with LBBB, examined with MPS and cardiac magnetic resonance (CMR), were included. Tracer uptake on MPS was classified by visual interpretation as typical LBBB pattern (Defect+, n = 13) or not (Defect−, n = 10) and quantitatively. CMR images were evaluated for wall thickness and for myocardial wall motion both by visual assessment and by regional myocardial radial strain from feature tracking, and for presence and location of myocardial fibrosis. ECGs were analyzed regarding QRS duration and the presence of strict criteria for LBBB. ResultsWall thickness was slightly lower in the septum compared to the lateral wall in Defect+ patients (5.6 ± 1.1 vs 6.0 ± 1.3 mm, P = 0.03) but not in Defect− patients (5.6 ± 1.0 vs 5.6 ± 0.9 mm, P = 0.84). Defect+ patients showed a larger proportion of dyskinetic segments in the septum and hyperkinetic segments in the lateral wall compared to Defect− patients (P = 0.006 and P = 0.004, respectively). Decreased myocardial radial strain was associated with decreased tracer uptake by MPS (R = 0.37, P < 0.001). Areas of fibrosis did not match areas with uptake defect on MPS. No differences in ECG variables were seen. ConclusionThe heterogeneous regional tracer uptake in some patients with LBBB is related to underlying regional myocardial dyskinesia, wall thickening, and wall thickness rather than stress-induced ischemia, myocardial fibrosis, or specific ECG characteristics.

Myocarditis, a Life-Threatening Presentation of COVID-19 in a 4-Month-Old Infant

Background and Aim: Significant cardiac sequelae may be one of the main causes of death in COVID-19 patients; however, very few reports are available that address these complications and their treatment strategies in children. Case Presentation: A 4-month-old male infant was admitted to the pediatric intensive care unit with sudden tachycardia, tachypnea, and low oxygen saturation after surgery. Laboratory tests and echocardiography revealed elevated troponin I levels and myocardial dyskinesia with decreased Left Ventricular Ejection Fraction (LVEF= 50%) and pulmonary hypertension (30 mm Hg) consistent with the cardiac injury. Despite his normal chest x-ray, the chest CT scan disclosed ground-glass opacities in the periphery of the left lower lobe indicative of viral infection. The patient fulfilled the diagnostic criteria of the “Chinese expert consensus statement for clinical myocarditis”. The viral test for COVID-19 obtained on the first day of admission was found positive a few days later. The patient successfully recovered clinically after receiving anti-failure therapy and IVIG. Trop I level reduced to 0.10 g/L, and the LVEF eventually recovered to 68%. Conclusion: COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure. Myocarditis in this patient was treated without antiviral drugs and only with supportive therapies.

Acute necrotizing encephalopathy and myocarditis in a young patient with COVID-19

A 33-year-old woman, previously healthy was admitted with generalized status epilepticus. Four days before, she had developed generalized fatigue, fever, headache, and nasal congestion. On hospital arrival, she was comatose (Glasgow coma scale 5 [E1/V1/M3]), febrile (38.6°C), tachycardic (145/min) with a blood pressure of 100/60 mm Hg, and tachypneic (35/min) with hypoxemia (pulse oximetry 80%). She was emergently intubated and started on mechanical ventilation and received IV midazolam and valproic acid for seizure control. Chest x-ray showed mild edema. The initial blood test results showed elevated myocardial enzymes; high-sensitivity troponin-I, 2,210 pg/mL; probrain natriuretic peptide, 992 pg/mL; creatine phosphokinase, 1858 mcg/L; and creatine kinase-MB, 22.5 ng/mL. Blood count revealed a white blood cell count of 14550/μL with absolute lymphopenia of 0.92/μL. C-reactive protein and erythrocyte sedimentation rate levels were high, whereas procalcitonin and lactic acid were normal. ECG showed sinus tachycardia and diffuse ST segment elevation. Bedside echocardiography showed diffuse myocardial dyskinesia with low left ventricular ejection fraction (29%) and small pericardial effusion. Head CT showed diffuse brain edema.

The Role of Phase Image in the Detection of Myocardial Dyskinesia by Magnetic Resonance Imaging (MRI).

The assessment of cardiac wall motion abnormalities plays an important role in the evaluation of many cardiovascular diseases and the prediction of functional recovery. Most of the methods dedicated to identifying the location of wall motion abnormalities have been restricted to study hypokinesia while an accurate way to assess dyskinesia is still needed in Cardiac Magnetic Resonance Imaging (CMRI). The aim of this study is to propose a phase image based on the analytic signal able to assess the extent of the myocardial dyskinetic segments in Cardiac Magnetic Resonance Imaging (CMRI). 22 subjects were retrospectively enrolled in this study (age 46 ± 11): 15 presenting an aneurysm and 7 control subjects with normal wall motion. For each patient, three standard views (short axis view, 2 chamber and 4 chamber views) were acquired using 3 Tesla Siemens Avanto MRI scanner and a segmented True FISP sequence. All the cine MRI images were analyzed by two experimented observers who were blinded to the diagnostic results. The outcomes of this study show that using the proposed phase image in MRI clinical routine can increase the accuracy of the detection of myocardial dyskinetic segments from 77.23 % to 86.38 %, the sensitivity from 67.48 % to 78.86 % as well the specificity from 80.92 % to 89.23 % compared to the standard method based on cine MRI interpretation. The phase image is a promising tool in CMRI for the assessment of dyskinetic segments and the degree of myocardial asynchronism.

Effect of Ranolazine on Ischemic Myocardium IN Patients With Acute Cardiac Ischemia (RIMINI-Trial): A Randomized Controlled Pilot Trial.

Coronary artery disease is the most prevalent manifestation among cardiovascular diseases. Despite modern treatment, risk of ischemic complications in patients with acute coronary syndrome (ACS) remains important. The late Na+ current blocker ranolazine has shown to reduce the risk of recurrent ischemia and worsening of angina in patients with non-ST-segment elevation ACS by possibly improving myocardial perfusion, but up to now no trial has addressed whether this enhanced perfusion also leads to a decrease in ischemic myocardium of patients with ACS. We designed a pilot trial (Reduction of Ischemic Myocardium with Ranolazine-Treatment IN patients with acute myocardial Infarction, ClinicalTrials.gov Identifier: NCT01797484) for feasibility and proof of concept that a 6-week ranolazine add-on therapy would reduce the area of ischemic myocardium in patients with ACS. The trial was designed in a 2-armed, controlled and randomized way. Twenty participants with unstable angina, proof of acute cardiac ischemia, and myocardial dyskinesia by speckle-tracking echocardiography were included. Ten participants received the study drug ranolazine additionally to standard treatment. The control group received standard treatment without additional study medication. Speckle-tracking echocardiography was performed before coronary intervention, before the first dose of ranolazine, and after 6 weeks of ranolazine treatment. Ranolazine was administered safely during acute myocardial infarction. Speckle-tracking echocardiography proved to be suitable for evaluation of myocardial dyskinesia. Patients receiving ranolazine showed a trend to higher normal fraction of the cumulative global strain than patients in the standard treatment group (15% vs 11%). No major complications relating study medication were observed. In conclusion, in this preliminary hypothesis-driven study, 6-week ranolazine therapy was shown to decrease the area of dyskinetic myocardium in patients with ACS by trend. Global strain rate measurement using speckle-tracking echocardiography can be applied measuring those effects and is, compared to other techniques, safe and harmless. Our data provide a sound basis for a follow-up trial.

Detecting Regional Myocardial Abnormalities in Patients With Wolff-Parkinson-White Syndrome With the Use of ECG-Gated Cardiac MDCT.

Myocardial dyskinesia caused by the accessory pathway and related reversible heart failure have been well documented in echocardiographic studies of pediatric patients with Wolff-Parkinson-White (WPW) syndrome. However, the long-term effects of dyskinesia on the myocardium of adult patients have not been studied in depth. The goal of the present study was to evaluate regional myocardial abnormalities on cardiac CT examinations of adult patients with WPW syndrome. Of 74 patients with WPW syndrome who underwent cardiac CT from January 2006 through December 2013, 58 patients (mean [± SD] age, 52.2 ± 12.7 years), 36 (62.1%) of whom were men, were included in the study after the presence of combined cardiac disease was excluded. Two observers blindly evaluated myocardial thickness and attenuation on cardiac CT scans. On the basis of CT findings, patients were classified as having either normal or abnormal findings. We compared the two groups for other clinical findings, including observations from ECG, echocardiography, and electrophysiologic study. Of the 58 patients studied, 16 patients (27.6%) were found to have myocardial abnormalities (i.e., abnormal wall thinning with or without low attenuation). All abnormal findings corresponded with the location of the accessory pathway. Patients with abnormal findings had statistically significantly decreased left ventricular function, compared with patients with normal findings (p < 0.001). The frequency of regional wall motion abnormality was statistically significantly higher in patients with abnormal findings (p = 0.043). However, echocardiography documented structurally normal hearts in all patients. A relatively high frequency (27.6%) of regional myocardial abnormalities was observed on the cardiac CT examinations of adult patients with WPW syndrome. These abnormal findings might reflect the long-term effects of dyskinesia, suggesting irreversible myocardial injury that ultimately causes left ventricular dysfunction.

Septal Dyskinesia and Global Left Ventricular Dysfunction in Pediatric Wolff‐Parkinson‐White Syndrome with Septal Accessory Pathway

Echocardiographic studies have shown that some patients with Wolff-Parkinson-White (WPW) syndrome have myocardial dyskinesia in the segments precociously activated by an accessory pathway (AP). The aim of the present study was to determine the extent to which the AP contributes to global left ventricular (LV) dysfunction. Electrophysiological and echocardiographic data from 62 children with WPW (age at diagnosis = 5.9 +/- 4.2 years) were retrospectively analyzed. The left ventricular ejection fraction (LVEF) of patients with septal APs (53 +/- 11%) was significantly lower than that of patients with right (62 +/- 5%) or left (61 +/- 4%) APs (P = 0.001). Compared to patients with normal septal motion (n = 56), patients with septal dyskinesia (n = 6) had a reduced LVEF (61 +/- 4% and 42 +/- 5%, respectively) and an increased LV end diastolic dimension (P < 0.001 for both comparisons). Multivariate analysis identified septal dyskinesia as the only significant risk factor for reduced LVEF. All 6 patients with septal dyskinesia had right septal APs, and a preexcited QRS duration that was longer than that of patients with normal septal motion (140 +/- 18 ms and 113 +/- 32 ms, respectively; P = 0.045). After RFA there were improvements in both intraventricular dyssynchrony (septal-to-posterior wall motion delay, from 154 +/- 91 ms to 33 +/- 17 ms) and interventricular septal thinning (from 3.0 +/- 0.5 mm to 5.3 +/- 2.6 mm), and a significant increase in LVEF (from 42 +/- 5% to 67 +/- 8%; P = 0.001). The dyskinetic segment activated by a right septal AP in WPW syndrome may lead to ventricular dilation and dysfunction. RFA produced mechanical resynchronization, reverse remodeling, and improvements in LV function.

Transesophageal echocardiography in patients with cryptogenic cerebral ischemia

BackgroundIn about one third of all patients with cerebral ischemia, no definite cause can be identified (cryptogenic stroke). In many patients with initially suspected cryptogenic stroke, however, a cardiogenic etiology can eventually be determined. Hence, the aim of this study was to describe the prevalence of abnormal echocardiographic findings in a large number of these patients.MethodPatients with cryptogenic cerebral ischemia (ischemic stroke, IS, and transient ischemic attack, TIA) were included. The initial work-up included a neurological examination, EEG, cCT, cMRT, 12-lead ECG, Holter-ECG, Doppler ultrasound of the extracranial arteries, and transthoracic echocardiography. A multiplane transeophageal echocardiography (TEE, including i.v. contrast medium application [Echovist], Valsalva maneuver) was performed in all patientsResults702 consecutive patients (380 male, 383 IS, 319 TIA, age 18–90 years) were included. In 52.6% of all patients, TEE examination revealed relevant findings. Overall, the most common findings in all patients were: patent foramen ovale (21.7%), previously undiagnosed valvular disease (15.8%), aortic plaques, aortic valve sclerosis, atrial septal aneurysms, regional myocardial dyskinesia, dilated left atrium and atrial septal defects. Older patients (> 55 years, n = 291) and patients with IS had more relevant echocardiographic findings than younger patients or patients with TIA, respectively (p = 0.002, p = 0.003). The prevalence rates of PFO or ASD were higher in younger patients (PFO: 26.8% vs. 18.0%, p = 0.005, ASD: 9.6% vs. 4.9%, p = 0.014).ConclusionA TEE examination in cryptogenic stroke reveals contributing cardiogenic factors in about half of all patients. Younger patients had a higher prevalence of PFO, whereas older patients had more frequently atherosclerotic findings. Therefore, TEE examinations seem indicated in all patients with cryptogenic stroke – irrespective of age – because of specific therapeutic consequences.

Segmental dyskinesia in Wolff–Parkinson–White syndrome: A possible cause of dilatative cardiomyopathy

Wolff–Parkinson–White (WPW) is a syndrome characterized by the presence of an accessory pathway that skipping A–V node may lead the electrical stimulus from the atrium directly to the ventricle. Some studies reported the finding of myocardial dyskinesia in the segments precociously activated by the accessory pathway, at echocardiogram and at nuclear cardiac study. Soria et al. reported, in 1985, an increased incidence of dilative cardiomyopathy in patients with WPW. The pathophysiological pathway that leads to ventricular dilation may be due to the increase of end-diastolic pressure secondary to a tachycardia-induced cardiomyopathy. Tachycardia-induced cardiomyopathy is usually secondary to frequent and prolonged tachycardia episodes. In this paper we report the cases of three patients affected by WPW who developed dilative cardiomyopathy during the follow-up. Particularly dyskinetic segments, working such as a functional aneurysm, could induce deep modifications of intraventricular haemodynamics, leading to remodelling and progressive ventricular dilation. This hypothesis could have important empirical consequences because it could imply the necessity of a precocious ablative therapy in this kind of patients.

Initiation of stress protein synthesis in the myocardium of coronary patients

We studied myocardial biopsy specimens from the right atrium of cardiological patients with different degree of cardiac ischemia obtained during surgery. No inducible HSP70 stress proteins were detected in atrial cardiomyocytes of patients with the WPW syndrome without signs of ischemic injuries of the heart. These proteins were detected in the myocardium of coronary patients. Their expression was more intense in patients with coronary disease paralleled by the development of myocardial dyskinesia. Two-dimensional electrophoresis showed only acid HSP70 but no alkaline isoforms in coronary patients even with pronounced dyskinesia. Presumably, alkaline HSP70 isoforms are present in the myocardium directly involved in the dyskinesia zone.

Xamoterol recruits an inotropic reserve in the acutely failing, reperfused canine myocardium without detrimental effects on its subsequent recovery

The present study tested (1) whether xamoterol recruits an inotropic reserve in reperfused myocardium and (2) whether acute inotropic stimulation by xamoterol has deleterious consequences on the long-term recovery of the reperfused myocardium. Sixteen anaesthetized, open-chest dogs were bilaterally vagotomized and heart rate kept constant by left atrial pacing. The distal left circumflex coronary artery was occluded for 15 min and then reperfused for 8 h. The coronary occlusion resulted in regional myocardial dyskinesia and myocardial function remained severely depressed after release of the occlusion. At 10 min reperfusion, 8 dogs received xamoterol (100 micrograms/kg i.v.), whereas the remaining 8 dogs served as controls and received saline. Xamoterol increased mean systolic wall thickening velocity (from 1.47 +/- 2.34 (SD) mm/s at 10 min reperfusion to 7.13 +/- 3.55 mm/s at 30 min reperfusion and 7.64 +/- 2.48 mm/s at 1 h reperfusion, respectively, both P less than 0.05). In the control group, only a slow recovery of mean systolic wall thickening velocity was observed (from 3.14 +/- 3.30 mm/s to 2.96 +/- 3.74 mm/s and 4.03 +/- 3.00 mm/s at 10 min, 30 min, and 1 h reperfusion, respectively). At 8 h reperfusion, mean systolic wall thickening velocity was similar in both groups (7.97 +/- 4.23 mm/s in the xamoterol-group and 6.87 +/- 4.00 mm/s in the placebo-group). Histological examination revealed no difference in the extent of necrosis between the two groups after 8 h reperfusion. We conclude that (1) xamoterol recruits an inotropic reserve in reperfused myocardium, and (2) this recruitment of an inotropic reserve does not compromise functional recovery and structural integrity of the reperfused myocardium.

Oxygen-Fentanyl Anesthesia in Patients with Poor Left Ventricular Function

Seven patients with poor left ventricular function (LVF) defined as ejection fraction less than 0.3, left ventricular end-diastolic pressure equal to or greater than 20 ton, and at least one area of myocardial dyskinesia, and 12 patients with good LVF scheduled for aortocoronary bypass surgery were anesthetized with a loading dose of 30 μg/kg fentanyl followed by infusion of fentanyl at a rate of 0.3 μg/kg/min until the start of rewarming on cardiopulmonary bypass. Premedication consisted of 0.15 mg/kg of diazepam orally and 0.15 mg/kg of morphine and 0.4 mg of scopolamine intramuscularly. Hemodynamic studies were obtained before and after induction and also after intubation, skin incision, sternotomy, and aortic dissection. Blood samples were taken for fentanyl radioimmunoassay before induction of anesthesia and 5, 10, 20, and 30 min after induction, and every 30 min thereafter. There were no significant differences in plasma fentanyl concentrations in the two groups. However, all patients with good LVF, as compared with only three of seven patients with poor LVF, became hypertensive. A significant number of patients (P < 0.05) with poor LVF did not develop hypertension because they appeared to have insufficient myocardial reserve to allow them to increase cardiac index in the face of an increase in systemic vascular resistance. We conclude that the study patients with both poor and good LVF anesthetized with a fentanyl infusion technique show similar plasma concentrations of fentanyl. We further conclude that such patients respond differently during induction of anesthesia and initial surgery and that this difference is a function of myocardial reserve rather than depth of anesthesia.

The Evaluation of Myocardial Dyskinesia in the Patients with Coronary Artery Diseases

The Evaluation of Myocardial Dyskinesia in the Patients with Coronary Artery Diseases

Detection of regional myocardial dyskinesia by ECG-gated, computerized radioisotope angiography

Detection of regional myocardial dyskinesia by ECG-gated, computerized radioisotope angiography