Guidelines for training in cardiovascular magnetic resonance (CMR).

These "Guidelines for training in Cardiovascular Magnetic Resonance" were developed by the Certification Committee of the Society for Cardiovascular Magnetic Resonance (SCMR) and approved by the SCMR Board of Trustees.

Pulmonary artery hemodynamics in primary pulmonary hypertension.

OBJECTIVES: The present investigation compared and contrasted steady and pulsatile pulmonary hemodynamics at rest and during exercise in patients with primary pulmonary hypertension and normal control subjects. BACKGROUND: A complete description of the relation between pressure and flow in the pulmonary circulation includes both steady and pulsatile hemodynamic behavior. Patients with primary pulmonary hypertension provide a unique opportunity to study the effects of primary alterations in pulmonary vasculature on pulmonary artery vascular hydraulic load. METHODS: Catheter tip pressure and velocity recordings from the main pulmonary artery in 8 patients with primary pulmonary hypertension and 10 control subjects were used to derive the pulmonary artery input impedance spectrum and the extent of pulse wave reflection at rest and during exercise. RESULTS: As expected, in patients with primary pulmonary hypertension, mean pulmonary artery pressure (50 +/- 10 mm Hg) and pulmonary vascular resistance (880 +/- 446 dynes.s.cm-5) were markedly elevated at rest and remained so during exercise (mean pressure 71 +/- 15 mm Hg, mean resistance 750 +/- 530 dynes.s.cm-5). Pulmonary artery characteristic impedance was elevated at rest and did not change with exercise (rest 55 +/- 25 dynes.s.cm-5; exercise 66 +/- 33 dynes.s.cm-5). Measures of arterial wave reflection indicated that the extent of wave reflection in the pulmonary bed in those with primary pulmonary hypertension is large at rest (reflection coefficient 0.89 +/- 0.09) and that the composite reflected wave arrived during the midportion of right ventricular ejection. Although the extent of wave reflection decreased with exercise (reflection coefficient 0.81 +/- 0.10, p < 0.05), the magnitude and timing of these reflections remained adverse. Furthermore, in patients with primary pulmonary hypertension, the stroke volume response to exercise was strongly related to rest levels of pulmonary artery diastolic pressure, pulmonary vascular resistance and the reflection factor, whereas no such relation was found in the control subjects. CONCLUSIONS: In addition to the expected abnormalities in steady measures of pulmonary artery hemodynamics at rest in patients with primary pulmonary hypertension, rest and exercise measures of oscillatory behavior (characteristic impedance and pulse wave reflection) are perturbed. Measures of steady and pulsatile behavior, particularly wave reflection, appear to have an important role in the exercise response of these patients.

Ultrafast three-dimensional contrast-enhanced magnetic resonance angiography and imaging in the diagnosis of partial anomalous pulmonary venous drainage.

OBJECTIVES: The purpose of our study was to evaluate patients with suspected anomalous pulmonary veins (APVs) and atrial septal defects (ASDs) using fast cine magnetic resonance imaging (MRI) and ultrafast three-dimensional magnetic resonance angiography (MRA). BACKGROUND: Precise anatomic definition of anomalous pulmonary and systemic veins, and the atrial septum are prerequisites for surgical correction of ASDs. Cardiac catheterization and transesophageal echocardiography (TEE) are currently used to diagnose APVs, but did not provide complete information in our patients. METHODS: Twenty consecutive patients with suspected APVs were studied by MRA after inconclusive assessment by catheterization, TEE or both. The MRI images were acquired with a fast cine sequence and a novel ultrafast three-dimensional sequence before and after contrast injection. RESULTS: Partial anomalous pulmonary venous drainage was demonstrated in 16 of 20 patients and was excluded in four patients. Magnetic resonance imaging correctly diagnosed APVs and ASDs in all patients (100%) who underwent surgery. For the diagnosis of APVs, the MRI and catheterization results agreed in 74% of patients and the MRI and TEE agreed in 75% of patients. For ASDs, MRI agreed with catheterization and TEE in 53% and 83% of patients, respectively. CONCLUSIONS: Fast cine MRI with three-dimensional contrast-enhanced MRA provides rapid and comprehensive anatomic definition of APVs and ASDs in patients with adult congenital heart disease in a single examination.

Angiotensin-converting enzyme inhibition limits dysfunction in adjacent noninfarcted regions during left ventricular remodeling.

OBJECTIVES: We hypothesized that angiotensin-converting enzyme inhibitors would limit dysfunction in the first 8 weeks after transmural infarction in adjacent noninfarcted regions, as well as attenuate left ventricular remodeling. BACKGROUND: Angiotensin-converting enzyme inhibition limits ventricular dilation and hypertrophy and improves survival after anterior infarction, but its effect on regional function during remodeling is not well characterized. METHODS: Thirteen sheep underwent coronary ligation to create an anteroapical infarction. At postinfarction day 2, eight sheep were randomized to therapy with the angiotensin-converting enzyme inhibitor ramipril, and five sheep received no therapy. Animals were studied with magnetic resonance myocardial tagging before and 8 weeks after infarction. Left ventricular volume, mass and ejection fraction were measured, as were changes in percent circumferential shortening within the subendocardium and subepicardium of infarcted and noninfarcted myocardium, both adjacent to and remote from the infarction. RESULTS: Angiotensin-converting enzyme inhibition limited the increase in end-diastolic volume from a mean (+/- SD) of +1.5 +/- 0.7 ml/kg in control animals to +0.5 +/- 0.8 ml/kg in the treated group (p < 0.04). Segmental function within infarcted and remote noninfarcted tissue did not differ between groups. However, angiotensin-converting enzyme inhibition limited the decline in function in the adjacent noninfarcted region 8 weeks after infarction. Percent circumferential shortening in the subendocardium decreased by -13 +/- 5% in the control group compared with -5 +/- 5% in the treated group (p < 0.03). CONCLUSIONS: In concert with a reduction in left ventricular remodeling after anterior infarction, angiotensin-converting enzyme inhibition limits the decline in function in the adjacent noninfarcted region. Dysfunction in adjacent noninfarcted regions may be an important determinant of left ventricular remodeling after infarction.

[Comparison of homogenous strain-analysis with wall thickening for the MR tomographic assessment of regional myocardial function]. / Homogene Strain-Analyse im Vergleich zur Wanddickenzunahme für die MR-tomographische Beurteilung der regionalen Myokardfunktion.

PURPOSE: To compare strain analysis and wall thickening (WT) analysis in differentiating the infarcted, adjacent, and remote zones in a rat model of myocardial infarction (MI). MATERIAL AND METHODS: Three normal (NL) and ten rats subjected to myocardial infarction were imaged on a 4.7T scanner. Gradient-echo and SPAMM-tagged cine images were acquired at three short axis levels of the left ventricle (LV). A homogenous strain analysis (principal strains lambda1 and lambda2, displacement D, angle beta) and a WT-analysis (mm- and %-thickening) were performed in all slices demonstrating MI. Regional function was compared between infarcted rats (infarcted, adjacent and remote zone) and corresponding regions in the NL rats. Additional segmental analysis was performed in the NL rats for the anterior, lateral, inferior and septal wall. RESULTS: In the NL rats, lambda (1) (greatest radial thickening) was greatest in the lateral and anterior wall. WT-analysis showed a pattern of function similar to lambda1, however, regional differences using WT-analysis were not significant. lambda (2) (greatest circumferential shortening) was most negative in the anterior wall. D was greatest in the lateral and inferior wall. The angle beta was radially directed in all segments. In the infarcted rats, both strain and WT-analyses revealed significant impairment in function in the infarcted and adjacent zones as compared to NL (p < 0.001). However, only the strain analysis (lambda1, lambda2, p < 0.001) detected significant remote myocardial dysfunction. Myocardial function differed significantly between the infarcted and adjacent and between the infarcted and remote regions. Strain analysis (lambda2, D, beta, p < 0.001) also identified significant functional differences between the adjacent and remote zones, however, no statistically significant differences were found using WT-analysis. CONCLUSION: Strain analysis is superior to WT-analysis in detecting regional functional variations in NL rats and in discriminating function in the infarcted, adjacent and remote zones post MI.

Right and left ventricular volume and ejection fraction by tomographic gated blood-pool scintigraphy.

UNLABELLED: Tomographic techniques separate overlying structures, permitting measurements of absolute ventricular volumes. The purpose of this study was to determine absolute right and left ventricular volume and ejection fraction measurements with tomographic gated equilibrium blood-pool scintigraphy (TMUGA) compared to MRI and conventional planar scintigraphy. METHODS: Eighteen patients were studied. Ventricular volumes for TMUGA and MRI were calculated by modified Simpson's rule. TMUGA regions were defined by constraints including phase analysis, intensity threshold and visual inspection. MRI studies were acquired with a fast gradient-echo, ECG-gated, breath-hold technique and boundaries were defined by a semiautomated contour method. Conventional gated first-pass radionuclide angiography (FP) and planar gated equilibrium blood-pool scintigraphy (PMUGA) were performed for RV EF and LV EF, respectively. RESULTS: TMUGA absolute right ventricular volumes showed excellent-correlation with MRI for both right ventricular volumes (r = 0.91, slope = 0.90, s.e.e. = 15.7) and left ventricular volumes (r = 0.96, slope = 0.88, s.e.e. = 18.2). For left ventricular ejection fraction, TMUGA also showed excellent correlation with MRI (r = 0.94, slope = 1.10, s.e.e. = 9.0) and planar MUGA (r = 0.97, slope = 1.23, s.e.e. = 6.2). For right ventricular ejection fraction, TMUGA showed good correlation with both MRI (r = 0.88, slope = 0.79, s.e.e. = 6.0) and first-pass planar scintigraphy (r = 0.86, slope = 1.2, s.e.e. = 7.9). CONCLUSION: Tomographic gated blood-pool scintigraphy absolute right and left ventricular volumes and ejection fractions show good correlation with accepted techniques. Further studies are necessary to define the reproducibility of this method.

Effect of dobutamine on regional left ventricular function measured by tagged magnetic resonance imaging in normal subjects.

The effect of inotropic stimulation on the pattern and magnitude of regional left ventricular contraction was studied using tagged magnetic resonance imaging to assess whether dobutamine exacerbates variation in regional contraction at rest. Dobutamine stress testing defines a normal response as a homogeneous increase in regional wall motion. In 8 normal subjects, 4 equally spaced left ventricular short-axis levels were imaged through systole using tagged magnetic resonance imaging. The baseline imaging sequence was repeated with 5-, 10-, 15-, and 20-microg/kg/min dobutamine infusion. Regional myocardial displacement, radial thickening, and circumferential shortening were measured. The left ventricle was analyzed by level (base to apex) and wall (septum, inferior, lateral, anterior). Dobutamine did not alter baseline regional functional heterogeneity. Dobutamine infusion resulted in a uniform increase in displacement, radial thickening, and circumferential shortening from baseline to 10-microg/kg/min infusion without additional increases at higher doses.

Extrinsic compression of the left main coronary artery by the pulmonary artery in patients with long-standing pulmonary hypertension.

Left main coronary artery compression by the pulmonary artery may be seen in patients with pulmonary hypertension who are undergoing cardiac catheterization. Cardiac magnetic resonance imaging is useful in these patients to document extrinsic compression, which might otherwise be mistaken for intrinsic atherosclerotic disease.

Structural determinants of aortic regurgitation in type A dissection and the role of valvular resuspension as determined by intraoperative transesophageal echocardiography.

Disruption of the aortic root by dissection often produces significant aortic regurgitation (AR). Resuspension of the native valve usually reestablishes competence. The mechanisms of this complex process are poorly understood. We used intraoperative transesophageal echocardiography to characterize the in vivo aortic root structure of type A aortic dissection and the changes brought about by native valve resuspension. Intraoperative transesophageal echocardiograms were obtained from 34 patients with type A dissection and aortic resuspension between January 1990 and April 1997. The severity of AR, aortic root diameter, circumference of the aortic annulus, percentage of the annulus dissected, and presence of leaflet prolapse were assessed in multiple planes. Preoperatively, AR of varying degree was present in 25 patients (73%). Multivariate analysis revealed that preoperative AR was most related to percentage of the annulus dissected (p<0.0001) and less related to root diameter (p<0.01). Leaflet prolapse was predicted by percent aortic annulus dissected (p <0.0001). After resuspension, annular dissection and leaflet prolapse were no longer present. Postoperative AR was significantly decreased from preoperative AR (p<0.0001) and was considered trace to mild. Although postoperative root diameter and annular circumference decreased (p<0.001), individual reductions in AR did not correlate with individual changes in root diameter or annular circumference. The degree of dissection of the valve annulus is the most significant determinant of leaflet prolapse and AR severity. Overall size of the aortic root also contributes to AR. Surgical resuspension significantly decreases root size, but its primary benefit is restoration of the structural integrity of the aortic annulus.

Pathogenesis of acute ischemic mitral regurgitation in three dimensions.

Changes in the geometric and intravalvular relationships between subunits of the ovine mitral valve were measured before and after acute posterior wall myocardial infarction in three dimensions by means of sonomicrometry array localization. In 13 sheep, nine sonomicrometer transducers were attached around the mitral anulus and to the tip and base of each papillary muscle. Five additional transducers were placed on the epicardium. Snares were placed around three branches of the circumflex coronary artery. One to 2 weeks later, echocardiograms, dimension measurements, and left ventricular pressures were obtained before and after the coronary arteries were occluded. Data were obtained from seven sheep. Coronary occlusion infarcted 32% of the posterior left ventricle and produced 2 to 3+ mitral regurgitation by Doppler color flow mapping. Multidimensional scaling of dimension measurements obtained from sonomicrometry transducers produced three-dimensional spatial coordinates of each transducer location throughout the cardiac cycle before and after infarction and onset of mitral regurgitation. After posterior infarction, the mitral anulus enlarges asymmetrically along the posterior anulus, and the tip of the posterior papillary muscle moves 1.5 +/- 0.3 mm closer to the posterior commissure at end-systole. The posterior papillary muscle also elongates 1.9 +/- 0.3 mm at end-systole. The left ventricle enlarges asymmetrically and ventricular torsion along the long axis changes. The development of postinfarction mitral regurgitation appears to be the consequence of multiple small changes in ventricular shape and contractile deformation and in the spatial relationship of mitral valvular subunits.

Estimation of total systemic arterial compliance in humans.

Systemic arterial compliance, a major component of aortic input impedance, was determined in 10 patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy and 11 age-matched control subjects found free of detectable cardiovascular disease. Total arterial compliance was determined from high-fidelity ascending aortic pressure and velocity recordings using 1) the traditional monoexponential aortic diastolic pressure decay and 2) the direct solution of the equation, which describes the three-element windkessel model of the arterial system. Resting values for total arterial compliance (x10(-3) cm5/dyn) derived from method 1 were significantly correlated with compliance derived from method 2 (r = 0.89, P less than 0.01). However, method 1 values (control mean 1.15 +/- 0.27, heart failure mean 1.18 +/- 0.54) were consistently and significantly lower (P less than 0.001) than method 2 values (control mean 1.59 +/- 0.50, heart failure mean 1.38 +/- 0.60). Resting total arterial compliance in heart-failure patients was not significantly different from control subjects. Total arterial compliance did not significantly change with exercise in either group despite increases in arterial pressure. However, nitroprusside administration in the heart-failure group increased total arterial compliance both at rest and on exercise compared with the unmedicated state. These different methodological approaches to the estimation of total arterial compliance in humans resulted in significantly different absolute values for compliance, although both methods provided concordant results with respect to the response of arterial compliance to physiological and pharmacological interventions.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis of a persistent coronary fistula after ventricular septal defect patch closure.

Penetrating chest trauma can result in multiple clinical syndromes depending on the structures involved. Tamponade, valvular regurgitation, ventricular septal defect (VSD), conduction system abnormalities, and coronary lacerations have been reported. We report a case of right ventricular free wall laceration, VSD, and coronary artery fistula involving a septal perforator.

Right ventricular dysplasia in an asymptomatic young man: an uncommon case with biventricular involvement and no known family history.

A 33-year-old man had cardiomegaly on a routine x-ray examination. He was asymptomatic with no history of infarction, syncope, or palpitations. There was no family history of congenital heart disease or sudden death. Two-dimensional transthoracic echocardiography demonstrated marked enlargement of the right atrium and ventricle with severely depressed right and left ventricular function that was consistent with right ventricular dysplasia. The patient was treated with an angiotensin-converting enzyme inhibitor and did well for 6 months, but then developed symptomatic left-sided congestive heart failure. Short-term improvement was obtained with intravenous inotropic therapy, but he continued to have progressive symptoms of heart failure. Approximately 7 months after his initial presentation, the patient underwent orthotopic heart transplantation for intractable congestive heart failure. Pathologic examination of the explanted heart established the diagnosis of right ventricular dysplasia with left ventricular involvement. This is an uncommon presentation of right ventricular dysplasia with biventricular involvement and no known family history.

Assessment of synchronized direct mechanical ventricular actuation in a canine model of left ventricular dysfunction.

Direct mechanical ventricular actuation (DMVA) is an experimental procedure that provides biventricular cardiac assistance by intracorporeal pneumatic compression of the heart. The advantages this technique has over other assist devices are biventricular assistance, no direct blood contact, pulsatile blood flow, and rapid, less complicated application. Prior studies of nonsynchronized DMVA support have demonstrated that a subject can be maintained for up to 7 days. The purpose of this study was to determine the acute hemodynamic effects of cardiac synchronized, partial DMVA support in a canine model (RVP) of left ventricular (LV) dysfunction. The study consisted of rapidly pacing seven dogs for 4 weeks to create LV dysfunction. At the conclusion of the pacing period, the DMVA device was positioned around the heart by means of a median sternotomy. The animals were then imaged in a 1.5 T whole body high speed clinical MR system, with simultaneous LV pressure recording. Left ventricular pressure-volume (PV) loops of the nonassisted and DMVA assisted heart were generated and demonstrated that DMVA assist shifted the loops leftward. In addition, assist significantly improved pressure dependent LV systolic parameters (left ventricular peak pressure and dp/dt max, p < 0.05), with no diastolic impairment. This study demonstrates that DMVA can provide synchronized partial assist, resulting in a decrease in the workload of the native heart, thus having a potential application for heart failure patients.

Acute systolic and diastolic indices of left ventricular function after cardiomyoplasty in a chronic model of heart failure.

Recent experimental studies have suggested that the initial nonstimulated stage of dynamic cardiomyoplasty acutely impairs ventricular function. Those investigations were performed on normal hearts and primarily examined diastolic alterations as a result of the passive muscle wrap. The purpose of this study was to assess the acute systolic and diastolic effects of a nonstimulated muscle wrap in chronic heart failure induced by rapid ventricular pacing in canines. Pressure-volume analysis of ventricular function based on conductance catheter volume and micromanometer pressure data was used. Each animal was studied before rapid pacing, before cardiomyoplasty, and immediately after wrap. By the end of the pacing period and before wrap, left ventricular dysfunction developed in all dogs, manifested by significant deterioration of both systolic and diastolic indices of ventricular function, as well as progressive increases in left ventricular volumes. However, no further deterioration with load insensitive indices of systolic or diastolic indicators of ventricular function was found as a result of the passive muscle wrap. These results suggest that the cardiomyoplasty procedure can be safely performed on failing hearts without prohibitive acute impairment of ventricular function.

Dynamic cardiomyoplasty decreases myocardial workload as assessed by tissue tagged MRI.

The effects of dynamic cardiomyoplasty (CMP) on global and regional left ventricular (LV) function in end-stage heart failure still remain unclear. MRI with tissue-tagging is a novel tool for studying intramyocardial motion and mechanics. To date, no studies have attempted to use MRI to simultaneously study global and regional cardiac function in a model of CMP. In this study, we used MRI with tissue-tagging and a custom designed MR compatible muscle stimulating/pressure monitoring system to assess long axis regional strain and displacement variations, as well as changes in global LV function in a model of dynamic cardiomyoplasty. Three dogs underwent rapid ventricular pacing (RVP; 215 BPM) for 10 weeks; after 4 weeks of RVP, a left posterior CMP was performed. After 1 year of dynamic muscle stimulation, the dogs were imaged in a 1.5 T clinical MR scanner. Unstimulated and muscle stimulated tagged long axis images were acquired. Quantitative 2-D regional image analysis was performed by dividing the hearts into three regions: apical, septal, and lateral. Maximum and minimum principal strains (lambda, and lambda2) and displacement (D) were determined and pooled for each region. MR LV pressure-volume (PV) loops were also generated. Muscle stimulation produced a leftward shift of the PV loops in two of the three dogs, and an increase in the peak LV pressure, while stroke volume remained unchanged. With stimulation, lambda1 decreased significantly (p<0.05) in the lateral region, whereas lambda2 increased significantly (p<0.05) in both the lateral and apical regions, indicating a decrease in strain resulting from stimulation. D only increased significantly (p<0.05) in the apical region. The decrease in strain between unassisted and assisted states indicates the heart is performing less work, while maintaining stroke volume and increasing peak LV pressure. These findings demonstrate that the muscle wrap functions as an active assist, decreasing the workload of the heart, while preserving total pump performance.

Determination of global function and regional mechanics of dynamic cardiomyoplasty using magnetic resonance imaging.

This study used tissue tagged magnetic resonance (MR) to assess regional strain and generate pressure-volume (PV) loops in a canine model of cardiomyoplasty (CMP). Three dogs with rapid ventricular pacing induced heart failure underwent dynamic CMP chronic cardiac assistance for 1 year. At the end of the study period, we performed a MR study with the myostimulator "on" and "off" and recording of left ventricular (LV) pressure. We determined the short axis displacement (D) and maximal and minimal principal strains (lambda1 and lambda2) by quantitative two-dimensional regional spatial modulation of magnetization visualization utility image analysis. LV PV loops were generated by combining the LV volume data from the MR images with the LV pressure recorded during imaging. Muscle stimulation produced a leftward shift of the LV PV loops in two of the three dogs, and an increase in LV peak pressure and dp/dt max. In contrast, short axis lambda1 and lambda2 did not change significantly (p = NS). D increased significantly in the anterolateral, posterolateral, and posteroseptal regions (p < 0.05) but did not change for the septal region (p = NS). Flap stimulation augments LV function in the absence of short axis strain change; this suggests that dynamic CMP exerts its main action along the long axis of the heart.

Prevalence and clinical relevance of the morphological substrate of ventricular arrhythmias in patients without known cardiac conditions detected by cardiovascular MR.

OBJECTIVE: Cardiac MR (CMR) identifies the substrate of ventricular arrhythmia (VA) in cardiomyopathies and coronary heart disease. However, little is known about the value of CMR in patients with VA without previously known cardiac disorders. METHODS: 76 patients with VA (Lown ≥2) without known cardiac disease after regular diagnostic work-up were studied with CMR, and findings were correlated with electrocardiogram (ECG) and electrophysiological stimulation (EPS). Structural abnormalities matching the VA origin as defined by ECG and/or EPS, or a CMR-detected cardiac condition known to cause arrhythmia were defined as VA substrate. CMR findings were defined as clinically relevant, if resulting in a new diagnosis, change of treatment or additional diagnostic procedure. RESULTS: 44/76 patients demonstrated pathological CMR findings. In 24/76 patients, the pathology was detected by CMR and not by echocardiography. CMR-based diagnoses of cardiac disease were established in 20/76 patients, and all were morphological substrates for VA. In seven patients, the location of the CMR finding (scar) directly matched the VA origin. CMR findings resulted in a change of treatment in 21 patients and/or additional diagnostics in 8 patients. CONCLUSION: Undetected cardiac conditions are frequent causes of VA. This is the first study demonstrating the value of CMR for detection of morphological substrate and/or underlying cardiac disorders in VA patients without known cardiac disease. ADVANCES IN KNOWLEDGE: The high incidence of clinically relevant CMR findings which were not detected during initial diagnostic work-up strongly supports the use of CMR to screen VA patients for underlying heart disease.