Coronary flow reserve is related to the extension and transmurality of myocardial necrosis and predicts functional recovery after acute myocardial infarction.

BACKGROUND: Few studies have examined the effect of transmurality of myocardial necrosis on coronary microcirculation. The aim of this study was to examine the influence of cardiac magnetic resonance-derived (GE-MRI) structural determinants of coronary flow reserve (CFR) after anterior myocardial infarction (STEMI), and their predictive value on regional functional recovery. METHODS: Noninvasive CFR and GE-MRI were studied in 37 anterior STEMI patients after primary coronary angioplasty. The wall motion score index in the left descending anterior coronary artery territory (A-WMSI) was calculated at admission and follow-up (FU). Recovery of regional left ventricular (LV) function was defined as the difference in A-WMSI at admission and FU. The necrosis score index (NSI) and transmurality score index (TSI) by GE-MRI were calculated in the risk area. Baseline (BMR) and hyperemic (HMR) microvascular resistance, arteriolar resistance index (ARI), and coronary resistance reserve (CRR) were calculated at the Doppler echocardiography. RESULTS: Bivariate analysis indicated that the CPK and troponin I peak, heart rate, NSI, TSI, BMR, the ARI, and CRR were related to CFR. Multivariable analysis revealed that TSI was the only independent determinant of CFR. The CFR value of >2.27, identified as optimal by ROC analysis, was 77% specific and 73% sensitive with accuracy of 76% in identifying patients with functional recovery. CONCLUSIONS: Preservation of microvascular function after AMI is related to the extent of transmurality of myocardial necrosis, is an important factor influencing regional LV recovery, and can be monitored by noninvasive CFR.

Coronary microvascular dysfunction induced by primary hyperparathyroidism is restored after parathyroidectomy.

BACKGROUND: Symptomatic primary hyperparathyroidism (PHPT) is associated with increased cardiovascular mortality. However, data on the association between asymptomatic PHPT and cardiovascular risk are lacking. We assessed coronary flow reserve (CFR) as a marker of coronary microvascular function in asymptomatic PHPT of recent onset. METHODS AND RESULTS: We studied 100 PHPT patients (80 women; age, 58±12 years) without cardiovascular disease and 50 control subjects matched for age and sex. CFR in the left anterior descending coronary artery was detected by transthoracic Doppler echocardiography, at rest, and during adenosine infusion. CFR was the ratio of hyperemic to resting diastolic flow velocity. CFR was lower in PHPT patients than in control subjects (3.0±0.8 versus 3.8±0.7; P<0.0001) and was abnormal (≤2.5) in 27 patients (27%) compared with control subjects (4%; P=0.0008). CFR was inversely related to parathyroid hormone (PTH) levels (r=-0.3, P<0.004). In patients with CFR ≤2.5, PTH was higher (26.4 pmol/L [quartiles 1 and 3, 16 and 37 pmol/L] versus 18 [13-25] pmol/L; P<0.007), whereas calcium levels were similar (2.9±0.1 versus 2.8±0.3 mmol/L; P=0.2). In multivariable linear regression analysis, PTH, age, and heart rate were the only factors associated with CFR (P=0.04, P=0.01, and P=0.006, respectively). In multiple logistic regression analysis, only PTH increased the probability of CFR ≤2.5 (P=0.03). In all PHPT patients with CFR ≤2.5, parathyroidectomy normalized CFR (3.3±0.7 versus 2.1±0.5; P<0.0001). CONCLUSIONS: PHPT patients have coronary microvascular dysfunction that is completely restored after parathyroidectomy. PTH independently correlates with the coronary microvascular impairment, suggesting a crucial role of the hormone in explaining the increased cardiovascular risk in PHPT.

Long-term outcome of morphology and function after soft tissue injury of the forearm with vascular involvement.

BACKGROUND: We sought to assess long-term changes in bone, muscle area, and muscle strength at different levels of the forearm and hand mobility according to arterial patency and nerve damage after surgically treated trauma related to involuntary local cutting/piercing injuries. METHODS: Forty subjects were evaluated 11 years after surgery for traumatic lesions involving the major vascular axis of the distal forearm. Peripheral quantitative computed tomography was used to measure cortical bone mineral density (BMD) and muscle area at the proximal radius, trabecular BMD at the distal radius, and cortical BMD at the third finger. Hand grip strength was assessed using dynamometry. Muscle area and hand grip strength were corrected for the limb dominance effect. RESULTS: All subjects had reduced trabecular BMD at the distal radius on the affected side (Δ, -5.8%; P < 0.001) and reduced cortical BMD in the third finger (Δ, -2.8%; P < 0.05). Hand grip strength was significantly lower on the affected side. According to vascular patency, only subjects with nonpreserved blood flow had significantly reduced distal radius BMD (Δ, -6.7%; P = 0.004), and those with nerve damage had a significant reduction in BMD at the third finger (Δ, -3.5%; P = 0.05). Moreover, nerve injury was associated with the presence of clinical symptoms and hand functional impairment. CONCLUSIONS: The absence of blood flow and nerve damage after forearm trauma caused by involuntary cutting/piercing injuries causes remarkable permanent impairment in musculoskeletal structures, hand grip strength, and hand functionality.

Relationship between myocardial blush grades, staining, and severe microvascular damage after primary percutaneous coronary intervention a study performed with contrast-enhanced magnetic resonance in a large consecutive series of patients.

BACKGROUND: Although angiographic perfusion has been traditionally evaluated by myocardial blush grade (MBG), pathophysiologic features underlying different MBG and the persistent blush, traditionally called staining, have been poorly explained. The aim of the study was to evaluate the correlation between MBG and morphologic aspects on cardiac magnetic resonance (CMR). METHODS: Myocardial blush grade and morphologic aspects on contrast-enhanced CMR, with special reference to staining phenomenon and persistent microvascular damage (PMD), were evaluated in a consecutive series of patients with acute myocardial infarction (AMI) treated by primary percutaneous coronary intervention. RESULTS: A total number of 294 AMI patients were enrolled and classified into 2 groups, that is, MBG 0/1 (115, 39%) and MBG 2/3 (179, 61%), according to the angiographic profile. By comparing MBG 0/1 versus MBG 2/3 patients, the former exhibited a larger enzymatic infarct size (P < .001) and a greater infarct size index (P < .001) and PMD (P < .001). In the MBG 0/1 group, a subgroup of 51 patients with staining phenomenon (MBG 0 staining) was also identified, with a worse CMR profile as PMD (P < .001). Multivariate analysis confirmed the strong association between MBG 0/1 and mean number of segments with transmural necrosis (odds ratio 1.62, 95% CI 1.17-2.24, P = .003) and PMD index (odds ratio 3.13, 95% CI 1.19-8.29, P = .021). CONCLUSIONS: In AMI patients treated by primary percutaneous coronary intervention, angiographic parameters of impaired reperfusion correlate with PMD as detected by contrast CMR. Among patients with MBG 0, the presence of the so-called staining phenomenon identifies a subgroup of patients with more severe PMD.

The contribution of intramyocardial hemorrhage to the "no-reflow phenomenon": a study performed by cardiac magnetic resonance.

BACKGROUND: Percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) is sometimes complicated by microvascular damage and hemorrhage. Hemoglobin degradation products have magnetic susceptibility effects which help in detecting hemorrhagic AMI by T2 -weighted cardiac magnetic resonance (CMR) images. OBJECTIVES: To investigate the possibility to detect intramyocardial hemorrhage after AMI and to assess its contribution to the delayed hypoenhanced core on late gadolinium enhancement (LGE) CMR, a feature traditionally referred to as microvascular obstruction. METHODS: Consecutive patients with AMI who underwent PCI and CMR were investigated. Hypointense zones T2 -weighted images were labelled as "hemorrhagic" AMI. Areas of late hypoenhancement on LGE CMR were considered as regions of persistent microvascular damage (PMD). Only transmural AMI were considered. RESULTS: A total number of 108 transmural AMI patients were eventually enrolled and divided into two groups according to the presence of hypoenhancement on T2 images. Thirty-two patients showed an hypointense stria within the high signal intensity zone on T2 -weighted images; all these patients showed midmural PMD on LGE. Among the remaining 76 patients, only 14 (18.4%) showed PMD in the subendocardial region. The angiographic outcome was worse in patients with hemorrhagic AMI, with a lower prevalence of TIMI 3 (65.6% vs. 96.1%, P = 0.017) and higher prevalence of myocardial blush grade 0 (84.4% vs. 13.2%, P < 0.001) post-PCI. CONCLUSIONS: T2 -weighted CMR in reperfused AMI allows identification of hemorrhage, related to PMD areas on LGE images and to a worse reperfusion profile on angiography. These features open new avenues of investigation for prognostic assessment of reperfused AMI.

Traumatic musculoskeletal changes in forearm and hand after emergency vascular anastomosis or ligation.

Whether the best option for the emergency treatment of major forearm artery lesions is anastomosis or ligation is still debated in the literature. The choice may be influenced by the resulting long-term musculoskeletal changes relating to vessel patency and the surgical procedure used. Fifty-three patients who had undergone emergency surgery involving arterial microanastomoses for lesions affecting one or more major forearm arteries (with a preserved distal circulation) were reassessed in terms of anastomosis patency at the end of a long-term follow-up, using arterial plethysmography, eco-color Doppler, and magnetic resonance angiography. In a subset of 40 patients, changes in bone mineral density (BMD) and lean mass of the affected limb were compared with the contralateral healthy limb and correlated with vessel patency and severity of trauma, using peripheral quantitative computed tomography and dual X-ray absorptiometry. Functional performance was also tested with a dynamometer by means of the hand-grip test. At long-term reassessment, 75% of the microanastomosed vessels were patent. BMD showed significant impairments at and around the site of the lesion (Delta: -6%, P < 0.001) and distally thereto (Delta: -3%, P < 0.05), which correlated with vessel occlusion and trauma severity. The fracture risk consequently also increased. There was evidence of a significant loss of lean mass ( P < 0.01) and muscle strength in the affected limb, especially in cases of occlusion of a major vessel. Given the satisfactory outcome of the anastomotic procedures as opposed to the greater loss of bone mass, muscular mass, and strength in patients who had undergone arterial ligation, we suggest that anastomosis is always preferable to ligation, even in emergencies. Anastomosis enables overall limb function to be better preserved (both in the vicinity of the lesion and distally).

Acute biopsy-proven lymphocytic myocarditis mimicking Takotsubo cardiomyopathy.

Endomyocardial biopsy (EMB), the diagnostic gold standard for myocarditis, has not been systematically performed in the reported case series of Takotsubo cardiomyopathy, although proposed Mayo Criteria specify exclusion of myocarditis. Moreover, there is no specific recommendation for infarct-like acute myocarditis in the recently published guidelines on the role of EMB. Here we present a thoroughly documented case fulfilling both the proposed Mayo criteria for Takotsubo cardiomyopathy and the World Health Organization criteria for active, virus-negative, immune-mediated myocarditis. Since myocarditis can mimic acute myocardial infarction with normal coronary arteries, EMB should be performed to rule out myocarditis in patients presenting with LV apical ballooning syndrome (or Takotsubo cardiomyopathy).

Periprocedural abciximab administration in ST elevation myocardial infarction patients. Effect on severe microvascular obstruction beyond the restoration of epicardial coronary flow by primary angioplasty.

OBJECTIVES: The impact of periprocedural (before primary percutaneous coronary angioplasty, PCI) abciximab administration on microvascular obstruction in patients with occluded infarct-related artery (IRA) is unknown. METHODS: We studied 36 consecutive patients with first ST elevation myocardial infarction (STEMI) and occluded IRA treated with successful primary PCI within 12 h from symptom onset, who received intravenous abciximab immediately before PCI and 49 matched patients who did not receive abciximab as controls. All patients underwent delayed-enhanced magnetic resonance (DE-MR) 6 +/- 2 days after PCI. Necrosis was judged as transmural when DE was extended to > or =75% of left ventricular (LV) segment thickness. Severe microvascular obstruction was identified as areas of late hypoenhancement surrounded by DE. RESULTS: Time to treatment was comparable in the two groups (182 +/- 60 vs. 188 +/- 110 min, respectively). Transmurality and severe microvascular obstruction were present in 3.03 +/- 2.8 versus 3.09 +/- 2.9 (p = 0.9) and 1.05 +/- 1.5 versus 1.06 +/- 1.8 (p = 0.6) of LV segments, respectively, in the abciximab group versus controls. At multivariate analysis, severe microvascular obstruction was independently associated only with transmural necrosis (OR 1.5, p < 0.001) and age (OR 1.1, p = 0.02) but not with the use of abciximab. CONCLUSIONS: Severe microvascular obstruction after primary PCI of STEMI patients with occluded IRA is related to transmural necrosis but not to the use of abciximab.

Correlation between magnetic resonance imaging and histopathological tumor response after neoadjuvant chemotherapy in breast cancer.

AIM: To evaluate the accuracy of magnetic resonance imaging in assessing tumor response following neoadjuvant chemotherapy in patients with locally advanced breast cancer. MATERIALS AND METHODS: Twenty-six patients entered a phase II study of neoadjuvant chemotherapy, undergoing bilateral breast magnetic resonance imaging before therapy and before surgery. Tumor response was classified using RECIST criteria, using tumor size at magnetic resonance imaging. The latter was then compared to residue found at histopathological examination. RESULTS: Magnetic resonance imaging showed 6 (23%) complete responses, 17 (65%) partial responses, 3 (11.5%) disease stabilizations and no disease progressions. Twenty-three tumors (88.5%) were considered responsive and 3 (11.5%) unresponsive. Pathological tumor response was: 6 complete responses (23%), 17 partial responses (65%), 2 stable disease (8%), 1 progression (4%). When results of the preoperative magnetic resonance imaging were compared to pathological tumor response, magnetic resonance imaging overestimated tumor size in 12 cases (46%) and underestimated it in 9 (35%). However, preoperative magnetic resonance imaging failed to detect invasive tumor in 2 false-negative cases (8%), 1 of which was multifocal. Mastectomy was performed in 12 cases: 1 case of disease progression even though the neoplasm appeared smaller at magnetic resonance imaging, 3 cases with stable disease, and 4 cases with T3 or T4 disease. The 9th patient was T2N2 with initial retroareolar disease and negative magnetic resonance imaging after chemotherapy. The 10th patient, affected by lobular cancer, was in partial remission but was T3N1. The 11th patient was 57 years old but was not interested in conservative surgery. The 12th patient requested bilateral prophylactic mastectomy due to her positive family history of breast cancer. CONCLUSIONS: Magnetic resonance imaging of the breast allowed conservative surgery in 54% of the patients. This low value is primarily due to overestimation of tumor size, with a negative predictive value of 67% in our population. However, surgeons were able to choose conservative surgery with relative safety in cases of small residual disease.

Morphologic validation of reperfused hemorrhagic myocardial infarction by cardiovascular magnetic resonance.

The purposes of this study were to assess the ex vivo cardiovascular magnetic resonance (CMR) signals of pathologically proved hemorrhagic myocardial infarction (MI) and to correlate these with in vivo CMR findings. Late gadolinium hypoenhancement within a hyperenhanced area in reperfused acute MI is ascribed to severe microvascular obstruction. The hearts of 2 patients, who died from cardiogenic shock after acute MIs and who had undergone coronary recanalization and in vivo CMR, were examined by T(2) and T(1) late enhancement sequences as well as by gross and histologic investigation. Four corresponding short-axis slices of each cardiac specimen from the base to the left ventricular apex were selected to assess the extent of MI and hemorrhage and were compared with the in vivo T(2) and late enhancement CMR scans. On pathologic examination, the extent of MI was 57 +/- 30% and 44 +/- 24%, and the extent of hemorrhage was 23 +/- 13% and 19 +/- 8% of the left ventricular area, respectively, showing progressive increases from the base to the apex. The low-signal intensity areas observed by ex vivo T(2) CMR strongly correlated with the hemorrhage quantified on histology (R = 0.93, p = 0.0007). Using ex vivo late gadolinium sequences, bright areas surrounded by thin dark rims, consistent with magnetic susceptibility effects, were detected, corresponding with hemorrhage. On in vivo CMR images, low-signal intensity and hyperintense areas with peripheral susceptibility artifacts were observed within the MI core on T(2) and late gadolinium sequences, respectively. In conclusion, in reperfused MI, CMR hypointense T(2) signal and susceptibility effects within the late gadolinium hypoenhanced areas are consistent with interstitial hemorrhage due to irreversible vascular injury, as proved by pathologic study.

Influence of transmurality, infarct size, and severe microvascular obstruction on left ventricular remodeling and function after primary coronary angioplasty.

Infarct size has been considered an established marker of left ventricular (LV) remodeling. We assessed the predictive value of myocardial/microvascular injury assessed by delayed enhanced magnetic resonance imaging (MRI) on LV remodeling and LV ejection fraction after primary coronary intervention (PCI) compared with peak troponin levels, an established index of myocardial infarct size. We performed MRI in 76 patients with first acute myocardial infarction 6 +/- 2 days after successful PCI. Necrosis was judged as transmural when delayed enhancement was extended to >or=75% of LV segment thickness. Severe microvascular obstruction was identified as areas of late hypoenhancement surrounded by delayed enhancement. Infarct size was expressed as an index by dividing the total percentage of delayed enhancement involvement by the number of LV segments. LV end-diastolic volume index and function were quantified by 2-dimensional echocardiography at 6 +/- 1 months after acute myocardial infarction. Remodeling was evaluated as a change in LV end-diastolic volume index at follow-up compared with baseline. At univariate analyses, transmural necrosis, severe microvascular obstruction, infarct size, and troponin level were correlated directly with remodeling and inversely with LV function at follow-up (p <0.001). At multiple regression, only transmural necrosis and troponin level remained independent predictors of LV remodeling and function. With respect to troponin, transmural necrosis improved the predictive power of LV remodeling (R2 for change = 0.19) and function (R2 for change = 0.16). In conclusion, in patients with acute myocardial infarction undergoing PCI, the amount of transmural necrosis as assessed by MRI is a major determinant of LV remodeling and function, with significant additional predictive value to infarct size and severe microvascular obstruction.

Unusual tumor-like calcification of the mitral annulus: diagnosis and tissue characterization by ultrasound, computed tomography and magnetic resonance imaging.

Calcification of the mitral annulus is a common echocardiographic finding in the elderly, particularly in females. Calcium deposits are generally located in the posterior mitral ring, sometimes extending to the whole mitral annulus and involving the mitral valve apparatus. The present report refers to 2 patients with a very atypical mass-like calcification of the mitral annulus resembling a cardiac tumor. A detailed evaluation of the mass was obtained at transthoracic and transesophageal echocardiography; the differential diagnosis with other intracardiac masses was aided by the use of computed tomography and magnetic resonance imaging. To our knowledge there has been no prior report of such a lesion evaluated at cardiac magnetic resonance imaging.

Myocardial crypt in an asymptomatic young athlete: how to interpret?

Myocardial crypts are extensions of blood signal penetrating the compact myocardium and are considered in literature as either a distinctive cardiac magnetic resonance (CMR) imaging marker for hypertrophic cardiomyopathy or as benign congenital malformations. What if CMR reveals a myocardial crypt in the presence of an altered ECG in an asymptomatic, enlarged young athlete's heart? The illustrated case demonstrates that new insights in CMR can also require further diagnostic interventions, which might have deleterious consequences for the individual athlete because of the uncertain interpretation of some findings in the demanding new world of a rapidly developing diagnostic imaging technique.

Impact of the presence and amount of myocardial fibrosis by cardiac magnetic resonance on arrhythmic outcome and sudden cardiac death in nonischemic dilated cardiomyopathy.

BACKGROUND: Current risk stratification for sudden cardiac death (SCD) in nonischemic dilated cardiomyopathy (NIDC) relies on left ventricular (LV) dysfunction, a poor marker of ventricular electrical instability. Contrast-enhanced cardiac magnetic resonance has the ability to accurately identify and quantify ventricular myocardial fibrosis (late gadolinium enhancement [LGE]). OBJECTIVE: To evaluate the impact of the presence and amount of myocardial fibrosis on arrhythmogenic risk prediction in NIDC. METHODS: One hundred thirty-seven consecutive patients with angiographically proven NIDC were enrolled for this study. All patients were followed up for a combined arrhythmic end point including sustained ventricular tachycardia (VT), appropriate implantable cardioverter-defibrillator (ICD) intervention, ventricular fibrillation (VF), and SCD. RESULTS: LV-LGE was identified in 76 (55.5%) patients. During a median follow-up of 3 years, the combined arrhythmic end point occurred in 22 (16.1%) patients: 8 (5.8%) sustained VT, 9 (6.6%) appropriate ICD intervention, either against VF (n = 5; 3.6%) or VT (n = 4; 2.9%), 3 (2.2%) aborted SCD, and 2 (1.5%) died suddenly. Kaplan-Meier analysis revealed a significant correlation between the LV-LGE presence (not the amount and distribution) and malignant arrhythmic events (P < .001). In univariate Cox regression analysis, LV-LGE (hazard ratio [HR] 4.17; 95% confidence interval [CI] 1.56-11.2; P = .005) and left bundle branch block (HR 2.43; 95% CI 1.01-5.41; P = .048) were found to be associated with arrhythmias. In multivariable analysis, the presence of LGE was the only independent predictor of arrhythmias (HR 3.8; 95% CI 1.3-10.4; P = .01). CONCLUSIONS: LV-LGE is a powerful and independent predictor of malignant arrhythmic prognosis, while its amount and distribution do not provide additional prognostic value. Contrast-enhanced cardiac magnetic resonance may contribute to identify candidates for ICD therapy not fulfilling the current criteria based on left ventricular ejection fraction.

Alström syndrome: cardiac magnetic resonance findings.

BACKGROUND: Alström Syndrome (ALMS) is an extremely rare multiorgan disease caused by mutations in ALMS1. Dilated cardiomyopathy (DCM) is a common finding but only one series has been investigated by Cardiac Magnetic Resonance (CMR). METHODS: Eight genetically proven ALMS patients (ages 11-41) underwent CMR performed by standard cine steady state, T1, T2 and late gadolinium enhancement (LGE) sequences. Ejection fraction (EF), Diastolic Volume (EDV) and Systolic Volume normalized for body surface area (ESV), and mass indices were determined, as well as EDV/Mass ratio, an index expressing the adequacy of cardiac mass to heart volume. Regional fibrosis was assessed by LGE; diffuse fibrosis was measured by a TI scout sequence acquired at 5, 10 and 15 min after gadolinium by comparing inversion time values (TI) at null time in ALMS and control group. RESULTS: In one patient severe DCM was present with diffuse LGE. There were seven cases without clinical DCM. In these patients, EF was at lower normal limits or slightly reduced and ESV index increased; six patients had decreased mass index and EDV/Mass ratio. Mild regional non ischemic fibrosis was detected by LGE in three cases; diffuse fibrosis was observed in all cases, as demonstrated by shorter TI values in ALMS in comparison with controls (5 min: 152 ± 12 vs 186 ± 16, p 0.0002; 10 min: 175 ± 8 vs 204 ± 18, p 0.0012; 15 min: 193 ± 9 vs 224 ± 16, p 0.0002). CONCLUSIONS: Cardiac involvement in ALMS is characterized by progressive DCM, associated with systolic dysfunction, myocardial fibrosis and reduced myocardial mass.

Apicobasal gradient of left ventricular myocardial edema underlies transient T-wave inversion and QT interval prolongation (Wellens' ECG pattern) in Tako-Tsubo cardiomyopathy.

BACKGROUND: Tako-Tsubo cardiomyopathy (TTC) presents with chest pain, ST-segment elevation followed by T-wave inversion and QT interval prolongation (Wellens' electrocardiographic [ECG] pattern), and left ventricular dysfunction, which may mimic an acute coronary syndrome. OBJECTIVE: To assess the pathophysiologic basis of the Wellens' ECG pattern in TTC by characterization of underlying myocardial changes by using cardiac magnetic resonance (CMR). METHODS: The study population included 20 consecutive patients with TTC (95% women; mean age 65.3 ± 10.4 years) who underwent CMR studies both in the initial phase and after 3-month follow-up by using a protocol that included cine images, T2-weighted sequences for myocardial edema, and post-contrast sequences for late gadolinium enhancement. Quantitative ECG indices of repolarization, such as maximal amplitude of negative T waves, sum of the amplitudes of negative T waves, and maximum corrected QT interval (QTc max), were correlated to CMR findings. RESULTS: At the time of initial CMR study, there was a significant linear correlation between the apicobasal ratio of T2-weighted signal intensity for myocardial edema and the maximal amplitude of negative T waves (ρ = 0.498; P = .02), sum of the amplitudes of negative T waves (ρ = 0.483; P = .03), and maximum corrected QT interval (ρ = 0.520; P = .02). Repolarization indices were unrelated to either late gadolinium enhancement or quantitative cine parameters. Wellens' ECG abnormalities and myocardial edema showed a parallel time course of development and resolution on initial and follow-up CMR studies. CONCLUSIONS: Our study results show that the ischemic-like Wellens' ECG pattern in TTC coincides and quantitatively correlates with the apicobasal gradient of myocardial edema as evidenced by using CMR. Dynamic negative T waves and QTc prolongation are likely to reflect the edema-induced transient inhomogeneity and dispersion of repolarization between apical and basal left ventricular regions.

LAD coronary artery myocardial bridging and apical ballooning syndrome.

OBJECTIVES: This study sought to evaluate the prevalence and potential role of myocardial bridging in the pathogenesis of apical ballooning syndrome (ABS). BACKGROUND: ABS is characterized by reversible left ventricular dysfunction, frequently precipitated by a stressful event, but the pathogenesis remains still unclear. METHODS: Forty-two consecutive patients (40 female, mean age 66 ± 7 years) with ABS underwent echocardiography, cardiac magnetic resonance, coronary angiography (CA) with intravascular ultrasound, and computed tomography angiography (CTA). Myocardial bridging was diagnosed by CA when a dynamic compression phenomenon was observed in the coronary artery and by CTA when a segment of coronary artery was completely (full encasement) or incompletely (partial encasement) surrounded by the myocardium. The prevalence of myocardial bridging detected by CTA and CA in ABS patients was compared with 401 controls without ABS who underwent both CTA and CA. RESULTS: Myocardial bridging by CTA was observed in 32 ABS patients (76%): 23 with partial encasement and 9 with full encasement. All myocardial bridging was located in the mid segment of the left anterior descending coronary artery (LAD) with a mean length of 17 ± 9 mm. CA revealed myocardial bridging in 17 subjects (40%) (9 with partial encasement and 8 with full encasement by CTA). All subjects in which dynamic compression was observed by CA showed myocardial bridging by CTA, while none of the subjects with negative findings for myocardial bridging by CTA revealed dynamic compression by CA. Compared with controls, ABS patients showed a significant higher prevalence of myocardial bridging in the LAD either by CA (40% vs. 8%; p < 0.001) or by CTA (76% vs. 31%; p < 0.001). CONCLUSIONS: Our study showed that myocardial bridging of the LAD is a frequent finding in ABS patients as revealed both by CA and, mostly, by CTA, suggesting a role of myocardial bridging as potential substrate in the pathogenesis of ABS.