Cardiovascular Magnetic Resonance Provides Evidence of Abnormal Myocardial Strain and Primary Cardiomyopathy in Marfan syndrome.

OBJECTIVE: Marfan syndrome is an autosomal-dominant genetic disorder caused by mutations in the fibrillin-1 gene. The condition is a connective tissue disease that frequently involves the cardiovascular system. The existence of a primary cardiomyopathy in Marfan syndrome, however, is controversial. The aims of this study were to investigate the prevalence of left ventricular dysfunction with both transthoracic echocardiography and cardiovascular magnetic resonance (CMR) in a cohort of Marfan syndrome patients and to investigate patterns of myocardial strain across the cohort. METHODS: We used an institutional database to identify all patients with a firm diagnosis of Marfan syndrome based on Ghent criteria. Inclusion required left ventricular ejection fraction (LVEF) to have been measured by both CMR and transthoracic echocardiography within 12 months of each other. Normal LVEF was defined as a value of >55% when measured by CMR. Velocity vector imaging was used to measure left ventricular longitudinal strain patterns by application of feature tracking to cine magnetic resonance images. Results were compared with data from 20 age-matched control subjects. RESULTS: Sixty-nine Marfan syndrome patients met the inclusion criteria. The mean age was 35.4 ± 15.0 years, and 56.5% were male. The mean LVEF was 59.0% ± 7.0% by CMR and 59.1% ± 5.8% by echo. One-fifth of Marfan syndrome patients (15/69; 21.7%) had reduced function with LVEF ≤55% by CMR, but only 5 of these were identified by echo. Furthermore, echo identified 5 Marfan syndrome patients as having reduced LVEF in the presence of a normal LVEF by CMR. Some Marfan syndrome patients had abnormal longitudinal strain patterns even with LVEF within the reference range. CONCLUSIONS: These data provide support for a primary cardiomyopathy in some Marfan syndrome patients. Cardiovascular magnetic resonance is more sensitive than echo for identifying cases with mild systolic dysfunction. Strain analysis may be more sensitive than simple LVEF assessment for identifying at-risk individuals.

Evaluation of the Clinical Utility of Transesophageal Echocardiography and Invasive Monitoring to Assess Right Ventricular Function During and After Pulmonary Endarterectomy.

OBJECTIVE: Patients undergoing pulmonary endarterectomy (PEA) have impaired right ventricular function. The authors sought to assess the clinical utility of commonly used perioperative echocardiographic and right heart catheter measurements in patients undergoing PEA. DESIGN: A single-center prospective observational study. SETTING: The study was conducted in a quaternary care cardiac surgical center in the United Kingdom. PARTICIPANTS: Patients undergoing PEA between April 2015 and January 2016. INTERVENTIONS: Thermodilution cardiac index and echocardiography variables were measured at 3 time points: before sternotomy (T1), after pericardial incision (T2), and after sternal closure (T3). Six-month follow-up echocardiography and 6-minute walk (6-MWT) test were performed. MEASUREMENTS AND MAIN RESULTS: Fifty patients were recruited and complete data sets were available for 41 patients. Tricuspid annular plane systolic excursion declined after pericardial incision and cardiopulmonary bypass (T1: 15 ± 4 mm, T2: 13 ± 4 mm, T3: 7 ± 2 mm; p < 0.0001), returning to baseline 6 months postoperatively. Cardiac index (T1: 2.5 ± 0.7 L/min/m2, T2: 2.6 ± 0.6 L/min/m2, T3: 2.3 ± 0.5 L/min/m2; p = 0.07) and right ventricular fractional area change (T1: 36 ± 11%, T2: 40 ± 12%, T3: 40 ± 9%; p = 0.12) were preserved perioperatively. 6-MWT improved from baseline (294 ± 111 m) to follow-up (357 ± 107 m) (p < 0.001). Pulmonary vascular resistance at T3 correlated moderately with follow-up 6-MWT (R = -0.60). CONCLUSIONS: In patients undergoing PEA, invasive measurements and echocardiography assessment of right ventricular function are not interchangeable. Tricuspid annular plane systolic excursion is not a reliable measure of right ventricular function perioperatively. Pulmonary vascular resistance shows moderate correlation with postoperative functional capacity.

Patterns of CMR measured longitudinal strain and its association with late gadolinium enhancement in patients with cardiac amyloidosis and its mimics.

BACKGROUND: Regional variability of longitudinal strain (LS) has been previously described with echocardiography in patients with cardiac amyloidosis (CA), however, the reason for this variability is not completely evident. We sought to describe regional patterns in LS using feature-tracking software applied to cardiovascular magnetic resonance (CMR) cine images in patients with CA, hypertrophic cardiomyopathy (HCM), and Anderson-Fabry's disease (AFD) and to relate these patterns to the distribution of late gadolinium enhancement (LGE). METHODS: Patients with CA (n = 45) were compared to LV mass indexed matched patients with HCM (n = 19) and AFD (n = 19). Peak systolic LS measurements were obtained using Velocity Vector Imaging (VVI) software on CMR cine images. A relative regional LS ratio (RRSR) was calculated as the ratio of the average of the apical segmental LS divided by the sum of the average basal and mid-ventricular segmental LS. LGE was quantified for the basal, mid, and apical segments using a threshold of 5SD above remote myocardium. A regional LGE ratio was calculated similar to RRSR. RESULTS: Patients with CA had significantly had worse global LS (-15.7 ± 4.6%) than those with HCM (-18.0 ± 4.6%, p = 0.046) and AFD (-21.9 ± 5.1%, p < 0.001). The RRSR was higher in patients with CA (1.00 ± 0.31) than in AFD (0.79 ± 0.24; p = 0.018) but not HCM (0.84 ± 0.32; p = 0.114). In CA, a regional difference in LGE burden was noted, with lower LGE in the apex (31.5 ± 19.1%) compared to the mid (38.2 ± 19.0%) and basal (53.7 ± 22.7%; p < 0.001 for both) segments. The regional LGE ratio was not significantly different between patients with CA (0.33 ± 0.15) and AFD (0.47 ± 0.58; p = 0.14) but lower compared to those with HCM (0.72 ± 0.43; p < 0.0001). LGE percentage showed a significant impact on LS (p < 0.0001), with a 0.9% decrease in absolute LS for every 10% increase in LGE percentage. CONCLUSION: The presence of marked "relative apical sparing" of LS along with a significant reduction in global LS seen in patients with CA on CMR cine analysis may provide an additional tool to differentiate CA from other cause of LVH. The concomitant presence of a base to apex gradient in quantitative LGE burden suggests that the regional strain gradient may be at least partially explained by the burden of amyloid deposition and fibrosis.

Left atrial and ventricular systolic and diastolic myocardial mechanics in patients with end-stage renal disease.

BACKGROUND: Diastolic cardiac dysfunction is an important complication of end-stage renal disease (ESRD), but quantification remains a challenge. Given that diastolic dysfunction is reflected in both left atrial (LA) and ventricular (LV) function, we aimed to identify abnormalities in LV and LA volume and function using measures of myocardial mechanics. METHODS: We retrospectively studied 53 incident ESRD patients (46±16 y/o 44% male) and compared them to 85 normal controls. LA phasic volumes and functional parameters were obtained from the apical 4CH view. Global ventricular peak longitudinal and circumferential strain, strain rate (GLS, GL-SR, CS), and rotation were obtained from apical and short-axis views. LA and LV measurements were taken off line using dedicated software (eSie VVI). RESULTS: ESRD patients had abnormal systolic function with lower LV ejection fraction and peak endocardial strain parameters (mean: GLS -16.6% vs -19.9%, GL-SR -0.91 vs -1.04, and CS -25.6% vs 27.9%, P≤.01 for all). Traditional Doppler parameters remained similar between groups, while diastolic mechanics were abnormal in ESRD. Reduced LV-derived diastolic parameters, fractional early reverse rotation, a marker of ventricular relaxation (P<.006), and ratio of early diastolic SR to systolic SR (P<.04) denote significant diastolic dysfunction. Increased LA volumes (P<.001), decreased LA reservoir (P<.001), conduit (P<.0004), and contractile (P<.02) function reflect diastolic dysfunction. CONCLUSION: Myocardial strain measurements quantitated the abnormalities in both LV diastolic and LA function associated with the uremic state. The distinct abnormal diastolic parameters were suggestive of abnormal relaxation and increased filling pressures. Early and accurate assessment of diastolic function may help tailor patient management ESRD.

The role of echocardiography in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a disease with a constellation of unique clinical, hemodynamic and echocardiographic features. Over the past decades, echocardiography has played a pivotal role in our understanding of the epidemiology, pathophysiology and prognosis of the condition. Recent advances in echocardiographic techniques have not only expanded our knowledge base but have also extrapolated the role of imaging from that of diagnosis, screening and non-invasive serial assessment to identification of poor prognostic markers, differentiation from phenocopies of HCM and guidance of intraprocedural decision-making in both septal ethanol ablation and surgical myectomy. This article summarizes the recent advances in echocardiography pertaining to HCM.

Deep basal inferoseptal crypts occur more commonly in patients with hypertrophic cardiomyopathy due to disease-causing myofilament mutations.

PURPOSE: To determine the relationship between deep basal inferoseptal crypts and disease-causing gene mutations in hypertrophic cardiomyopathy (HCM). MATERIALS AND METHODS: Institutional research and ethics board approval was obtained for this retrospective study, and the requirement to obtain informed consent was waived. Two readers, who were blinded to genetic status, independently assessed cardiac magnetic resonance (MR) images obtained in 300 consecutive unrelated genetically tested patients with HCM. Readers documented the morphologic phenotype, the presence of deep basal inferoseptal crypts, and the imaging plane in which crypts were first convincingly visualized. The Student t test, the Fisher exact test, and multivariate logistic regression were used for comparisons and to evaluate the relationship between these crypts and the detection of disease-causing mutations. RESULTS: The frequency of deep basal inferoseptal crypts was significantly higher in patients with disease-causing mutations than in those without disease-causing mutations (36% and 4%, respectively; P < .001). The presence of crypts was a stronger predictor of disease-causing mutations than was reverse septal curvature (P = .025). Patients with these crypts had a higher likelihood of having disease-causing mutations than non-disease-causing mutations (P < .001). Thirty-one of the 34 patients with both deep basal inferoseptal crypts and reverse septal curvature (91%) had disease-causing mutations (sensitivity, 26%; specificity, 98%). The presence of deep basal inferoseptal crypts (odds ratio: 6.64; 95% confidence interval: 2.631, 16.755; P < .001) and reverse septal curvature (odds ratio: 4.8; 95% confidence interval: 2.552, 9.083; P < .001) were predictive of disease-causing mutations. Both observers required additional imaging planes to identify approximately half of all crypts. CONCLUSION: Deep basal inferoseptal crypts occur more commonly in patients with HCM with disease-causing mutations than in those with genotype-negative HCM.

Percutaneous Transcatheter Closure of Post-infarction Ventricular Septal Defect: An Alternative to Surgical Intervention.

Post-infarction ventricular septal defect is a mechanical complication of acute MI. The incidence of this complication is low in the primary percutaneous coronary intervention era. However, the associated mortality is very high at 94% with medical management alone. Open surgical repair or percutaneous transcatheter closure still has an in-hospital mortality >40%. Retrospective comparisons between both closure methods are limited by observation and selection bias. This review addresses the assessment and optimisation of patients prior to repair, the optimal timing of repair, and the limitations in current data. The review considers techniques for percutaneous closure, and finally considers the path that future research should take to improve outcomes for patients.

Glucose-insulin-potassium reduces the incidence of low cardiac output episodes after aortic valve replacement for aortic stenosis in patients with left ventricular hypertrophy: results from the Hypertrophy, Insulin, Glucose, and Electrolytes (HINGE) trial.

BACKGROUND: Patients undergoing aortic valve replacement for critical aortic stenosis often have significant left ventricular hypertrophy. Left ventricular hypertrophy has been identified as an independent predictor of poor outcome after aortic valve replacement as a result of a combination of maladaptive myocardial changes and inadequate myocardial protection at the time of surgery. Glucose-insulin-potassium (GIK) is a potentially useful adjunct to myocardial protection. This study was designed to evaluate the effects of GIK infusion in patients undergoing aortic valve replacement surgery. METHODS AND RESULTS: Patients undergoing aortic valve replacement for aortic stenosis with evidence of left ventricular hypertrophy were randomly assigned to GIK or placebo. The trial was double-blind and conducted at a single center. The primary outcome was the incidence of low cardiac output syndrome. Left ventricular biopsies were analyzed to assess changes in 5' adenosine monophosphate-activated protein kinase (AMPK), Akt phosphorylation, and protein O-linked ß-N-acetylglucosamination (O-GlcNAcylation). Over a 4-year period, 217 patients were randomized (107 control, 110 GIK). GIK treatment was associated with a significant reduction in the incidence of low cardiac output state (odds ratio, 0.22; 95% confidence interval, 0.10 to 0.47; P=0.0001) and a significant reduction in inotrope use 6 to 12 hours postoperatively (odds ratio, 0.30; 95% confidence interval, 0.15 to 0.60; P=0.0007). These changes were associated with a substantial increase in AMPK and Akt phosphorylation and a significant increase in the O-GlcNAcylation of selected protein bands. CONCLUSIONS: Perioperative treatment with GIK was associated with a significant reduction in the incidence of low cardiac output state and the need for inotropic support. This benefit was associated with increased signaling protein phosphorylation and O-GlcNAcylation. Multicenter studies and late follow-up will determine whether routine use of GIK improves patient prognosis.

Percutaneous management of paravalvular leaks.

Paravalvular leak (PVL) is a challenging complication of valve replacement surgery that can cause heart failure and haemolysis. Surgical repair is the traditional treatment for severe, symptomatic PVL, but many patients with PVL fall into high-risk categories for redo surgery. Percutaneous techniques for closure of PVL have been increasingly refined over the last decade with availability of approved purpose-specific devices for closure. Percutaneous closure requires a heart team approach, with attention paid to appropriate preprocedural and periprocedural imaging to ensure a successful closure with minimal residual leak or complication. There are limited studies addressing the selection of a percutaneous approach to PVL. No randomised trials comparing surgical and percutaneous repair have been conducted. Large national registries from the UK and Ireland and from Spain have demonstrated that high rates of technical success can be achieved, with mortality comparable with surgical repair. Six retrospective studies comparing surgical and percutaneous approaches have been published. These broadly show comparable technical success between the interventions, with reduced short-term mortality among patients treated percutaneously. Long-term outcomes were similar between both treatment options. Percutaneous repair is an attractive treatment option in many patients due to its reduced invasiveness and quicker recovery period. However, more prospective studies are needed to validate its place in the armamentarium of the heart team.

Short-term hemodynamic effects of cardiac resynchronization therapy in patients with heart failure, a narrow QRS duration, and no dyssynchrony.

BACKGROUND: Cardiac resynchronization therapy produces both short-term hemodynamic and long-term symptomatic/mortality benefits in symptomatic heart failure patients with a QRS duration >120 ms. This is conventionally believed to be due principally to relief of dyssynchrony, although we recently showed that relief of external constraint to left ventricular filling may also play a role. In this study, we evaluated the short-term hemodynamic effects in symptomatic patients with a QRS duration <120 ms and no evidence of dyssynchrony on conventional criteria and assessed the effects on contractility and external constraint. METHODS AND RESULTS: Thirty heart failure patients (New York Heart Association class III/IV) with a left ventricular ejection fraction < or =35% who were in sinus rhythm underwent pressure-volume studies at the time of pacemaker implantation. External constraint, left ventricular stroke work, dP/dtmax, and the slope of the preload recruitable stroke work relation were measured from the end-diastolic pressure-volume relation before and during delivery of biventricular and left ventricular pacing. The following changes were observed during delivery of cardiac resynchronization therapy: Cardiac output increased by 25+/-5% (P<0.05), absolute left ventricular stroke work increased by 26+/-5% (P<0.05), the slope of the preload recruitable stroke work relation increased by 51+/-15% (P<0.05), and dP/dtmax increased by 9+/-2% (P<0.05). External constraint was present in 15 patients and was completely abolished by both biventricular and left ventricular pacing (P<0.05). CONCLUSIONS: Cardiac resynchronization therapy results in an improvement in short-term hemodynamic variables in patients with a QRS <120 ms related to both contractile improvement and relief of external constraint. These findings provide a potential physiological basis for cardiac resynchronization therapy in this patient population.

Patent Foramen Ovale Closure: State of the Art.

Patent foramen ovale (PFO) is a common abnormality affecting between 20% and 34% of the adult population. For most people, it is a benign finding; however, in some people, the PFO can open widely to enable paradoxical embolus to transit from the venous to arterial circulation, which is associated with stroke and systemic embolisation. Percutaneous closure of the PFO in patients with cryptogenic stroke has been undertaken for a number of years, and a number of purpose-specific septal occluders have been marketed. Recent randomised control trials have demonstrated that closure of PFO in patients with cryptogenic stroke is associated with reduced rates of recurrent stroke. After a brief overview of the anatomy of a PFO, this article considers the evidence for PFO closure in cryptogenic stroke. The article also addresses other potential indications for closure, including systemic arterial embolisation, decompression sickness, platypnoea-orthodeoxia syndrome and migraine with aura. The article lays out the pre-procedural investigations and preparation for the procedure. Finally, the article gives an overview of the procedure itself, including discussion of closure devices.

Echocardiography in the Diagnosis and Management of Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is an inherited condition present in about 1/500 individuals with more than 1500 causative mutations identified in primarily 10 sarcomeric proteins. Although HCM is inherited in an autosomal dominant way, there is often incomplete penetrance and variable phenotype even with the same genotype. It is characterized by a degree of hypertrophy (usually asymmetric), that is, not due to another identifiable cause, as well as variable degrees of myocardial fibrosis and microvascular abnormalities.

Multilayer Myocardial Mechanics in Genotype-Positive Left Ventricular Hypertrophy-Negative Patients With Hypertrophic Cardiomyopathy.

It is unknown whether the presence of a sarcomeric mutation alone is sufficient to result in abnormal myocardial force generation, or whether additional changes in myocardial architecture (hypertrophy, disarray, and fibrosis) are required to impair systolic function. Speckle tracking echocardiography allows quantification of global strain/strain rates, twist, and dyssynchrony. In the present study we sought to further elucidate early abnormalities of myocardial mechanics in sarcomeric mutation carriers without evidence of clinical disease. Sixty genotype-positive left ventricular hypertrophy-negative (G+left ventricular hypertrophy [LVH]-) patients and 60 normal controls were studied. Velocity vector imaging was applied retrospectively to echocardiographic images to quantify global longitudinal and circumferential strain/strain rate, and rotation parameters. The G+LVH- group demonstrated both smaller left ventricular diastolic cavity dimensions (4.5 ± 0.6 cm vs 4.8 ± 0.4 cm) and a higher LVEF (66 ± 6% vs 60 ± 5%) compared with controls. An increase in circumferential subendocardial systolic strain (-30 ± 5 vs -27 ± 3%) and both systolic and diastolic subendocardial strain rate was seen in the G+LVH- group. Peak rotation angles were higher at the base and apex, with an increase in total twist (9.0 ± 3.8 vs 6.9 ± 2.9). In the control group, global and average segmental strain were similar, suggesting no/minimal dyssynchrony (global mechanical synchrony index [GMSi] 0.97-0.98). In the G+LVH- group GMSi was significantly lower (subendocardial GMSi 0.95; subepicardial GMSi 0.60), suggesting increasing subendocardial to subepicardial dyssynchrony. In conclusion, utilizing multilayer strain analysis, we demonstrate that G+LVH- subjects have enhanced subendocardial systolic strain rate and twist, as well as mechanical dyssynchrony within the left ventricular myocardium. These results demonstrate that abnormalities in myocardial mechanics precede the development of clinical hypertrophy.

Comparison of echocardiographic parameters between pre-clinical and clinical advanced diastolic dysfunction patients.

BACKGROUND: The diagnosis of heart failure (HF) with preserved ejection fraction requires evidence of grade 2 or 3 (advanced) diastolic dysfunction (ADD), but many patients with ADD do not have clinical HF manifestations, hence termed pre-clinical diastolic dysfunction (PDD). The prevalence and characteristics of PDD in comparison to overt HF disease (clinical-ADD) are still debated. METHODS: We retrospectively analyzed 373 patients with LVEF≥45% and ADD in our echo-lab database. Exclusion criteria were acute coronary syndromes, ≥moderate valvular disease, cardiomyopathies or pericardial disease. Patients were divided into 2 groups according to the presence/absence of HF symptoms, namely PDD (n=249) and clinical-ADD (n=124). Demographic, clinical and echocardiographic parameters were compared between the groups. RESULTS: Age, gender and comorbidities were similar between groups, with only a higher body mass index and renal failure significantly more prevalent in the clinical-ADD patients. Neither LV mass nor the ADD severity was related to the presence of symptoms; lateral mitral E/E' and pulmonary artery systolic pressure were significantly higher in clinical-ADD patients (14±5 vs. 12±4, p<0.05 and 40±13 vs. 36±11mmHg, p<0.05, respectively) and were the only parameters to correlate with the presence of symptoms of clinical-ADD in multivariable logistic regression (odds ratio=1.07 (CI 1.02-1.1, p=0.008) and 1.03 (CI 1.01-1.05, p=0.01), respectively). CONCLUSIONS: In patients referred for an echocardiogram at a community cardiology center, PDD was twice as common as clinical-ADD. Hemodynamic parameters reflecting elevated filling and pulmonary pressures, rather than traditional comorbidities and/or classical structural abnormalities, were the only parameters related to the presence of HF symptoms.

Improvement in cardiac energetics by perhexiline in heart failure due to dilated cardiomyopathy.

OBJECTIVES: The aim of this study was to determine whether short-term treatment with perhexiline improves cardiac energetics, left ventricular function, and symptoms of heart failure by altering cardiac substrate utilization. BACKGROUND: Perhexiline improves exercise capacity and left ventricular ejection fraction (LVEF) in patients with heart failure (HF). (31)P cardiac magnetic resonance spectroscopy can be used to quantify the myocardial phosphocreatine/adenosine triphosphate ratio. Because improvement of HF syndrome can improve cardiac energetics secondarily, we investigated the effects of short-term perhexiline therapy. METHODS: Patients with systolic HF of nonischemic etiology (n = 50, 62 ± 1.8 years of age, New York Heart Association functional class II to IV, LVEF: 27.0 ± 1.44%) were randomized to receive perhexiline 200 mg or placebo for 1 month in a double-blind fashion. Clinical assessment, echocardiography, and (31)P cardiac magnetic resonance spectroscopy were performed at baseline and after 1 month. A substudy of 22 patients also underwent cross-heart blood sampling at completion of the study to quantify metabolite utilization. RESULTS: Perhexiline therapy was associated with a 30% increase in the phosphocreatine/adenosine triphosphate ratio (from 1.16 ± 0.39 to 1.51 ± 0.51; p < 0.001) versus a 3% decrease with placebo (from 1.36 ± 0.31 to 1.34 ± 0.31; p = 0.37). Perhexiline therapy also led to an improvement in New York Heart Association functional class compared with placebo (p = 0.036). Short-term perhexiline therapy did not change LVEF. Cross-heart measures of cardiac substrate uptake and respiratory exchange ratio (which reflects the ratio of substrates used) did not differ between patients who received perhexiline versus placebo. CONCLUSIONS: Perhexiline improves cardiac energetics and symptom status with no evidence of altered cardiac substrate utilization. No change in LVEF is seen at this early stage. (Metabolic Manipulation in Chronic Heart Failure; NCT00841139).

Effect of Left Ventricular Outflow Tract Obstruction on Left Atrial Mechanics in Hypertrophic Cardiomyopathy.

Left atrial (LA) volumes are known to be increased in hypertrophic cardiomyopathy (HCM) and are a predictor of adverse outcome. In addition, LA function is impaired and is presumed to be due to left ventricular (LV) diastolic dysfunction as a result of hypertrophy and myocardial fibrosis. In the current study, we assess the incremental effect of outflow tract obstruction (and concomitant mitral regurgitation) on LA function as assessed by LA strain. Patients with HCM (50 obstructive, 50 nonobstructive) were compared to 50 normal controls. A subset of obstructive patients who had undergone septal myectomy was also studied. Utilising feature-tracking software applied to cardiovascular magnetic resonance images, LA volumes and functional parameters were calculated. LA volumes were significantly elevated and LA ejection fraction and strain were significantly reduced in patients with HCM compared with controls and were significantly more affected in patients with obstruction. LA volumes and function were significantly improved after septal myectomy. LVOT obstruction and mitral regurgitation appear to further impair LA mechanics. Septal myectomy results in a significant reduction in LA volumes, paralleled by an improvement in function.

The effect of percutaneous coronary intervention of chronically totally occluded coronary arteries on left ventricular global and regional systolic function.

BACKGROUND: Percutaneous coronary intervention (PCI) is frequently attempted to open chronic total occlusions (CTOs) and restore epicardial coronary flow. Data suggest adverse outcomes in the case of PCI failure. We hypothesized that failure to open a CTO might adversely affect regional cardiac function and promote deleterious cardiac remodelling, and success would improve global and regional cardiac function assessed using cardiac magnetic resonance and velocity vector imaging. METHODS: Thirty patients referred for PCI to a CTO underwent cardiac magnetic resonance examination before and after the procedure. Left ventricular function and transmural extent of infarction was assessed in these patients. Regional cardiac function using Velocity Vector Imaging version 3.0.0 (Siemens) was assessed in 20 patients. RESULTS: Successful CTO opening (thrombolysis in myocardial infarction 3 flow) occurred in 63% of patients. Left ventricular ejection fraction significantly increased after successful PCI (50 ± 13% to 54 ± 11%; P < 0.01). Global longitudinal strain (GLS) fell significantly in the failed group (Δ = -25 ± 17%; P = 0.02) in contrast with successful PCI in which GLS did not change (Δ 20 ± 32%; P = 0.17). GLS rate followed a pattern similar to GLS (failed, Δ -30 ± 17%; P < 0.01 vs success Δ 25 ± 48%; P = 0.34). In contrast, radial and circumferential strain/strain rate were not different between groups after success/failed PCI. CONCLUSIONS: Regional cardiac function assessment using velocity vector imaging showed a significant decline in GLS and GLS rate in patients in whom PCI failed to open a CTO, with no change in global measures of cardiac function.

Velocity vector imaging in the measurement of left ventricular myocardial mechanics on cardiac magnetic resonance imaging: correlations with echocardiographically derived strain values.

BACKGROUND: Regional and global function can be measured by echocardiography using speckle-tracking, a technique that has previously been validated against crystal sonomicrometry. However, the application of Velocity Vector Imaging (VVI) to images obtained from cardiac magnetic resonance (CMR) imaging has never been validated against those values derived from VVI applied to two-dimensional echocardiographic images in the same patient group. The aim of this study was to validate for the first time the application of VVI to retrospectively acquired CMR data sets for the assessment of left ventricular strain and rotation, using echocardiographic strain assessment by VVI as the reference technique. METHODS: Cine steady-state free precession CMR data sets and two-dimensional echocardiographic images obtained on the same day in 36 adult patients with hypertrophic cardiomyopathy were analyzed retrospectively using VVI to quantify global longitudinal and circumferential strain and rotation parameters. RESULTS: The absolute differences in longitudinal strain between the two imaging modalities were -1.1 ± 3.3% (endocardial) and -2.2 ± 3.6% (full thickness). The absolute differences in circumferential strain were -4.7 ± 5.3% (endocardial) and -3.4 ± 3.8% (full thickness). CMR consistently resulted in higher strain values than echocardiography. The absolute differences in twist were -0.2 ± 5.6% (endocardial) and 0.1 ± 5.8% (full thickness). CONCLUSIONS: The application of VVI to CMR data sets allows a feasible and reproducible method for strain analysis in HCM, demonstrating excellent agreement with two-dimensional echocardiography-derived values. Given the superior image quality obtained with CMR in a significant proportion of patients, this technique provides a method for strain assessment without the need for dedicated CMR acquisition and analytic techniques.