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.

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.

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.

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.

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.

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.

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.

Imaging study of ventricular scar in arrhythmogenic right ventricular cardiomyopathy: comparison of 3D standard electroanatomical voltage mapping and contrast-enhanced cardiac magnetic resonance.

BACKGROUND: The hallmark lesion of arrhythmogenic right ventricular cardiomyopathy (ARVC) is fibrofatty scar replacement. We compared endocardial voltage mapping (EVM) and contrast-enhanced cardiac magnetic resonance (CE-CMR) for imaging scar lesions in ARVC patients. METHODS AND RESULTS: We studied 23 consecutive ARVC patients (16 males; mean age, 38±12 years) who underwent RV EVM and CE-CMR and 37 control subjects. In 21 (91%) of 23 ARVC patients, RV EVM was abnormal, with a total of 45 electroanatomical scars (EAS): 17 (38%) in the inferobasal region, 12 (26.6%) in the anterolateral region, 8 (17.7%) in the RV outflow tract (RVOT), and 8 (17.7%) in the apex. RV delayed contrast enhancement (DCE) was found in 9 (39%) of 23 patients, with a total of 23 RV DCE scars: 4 (17.4%) in the inferobasal region, 9 (39.1%) in the anterolateral region, 4 (17.4%) in the RVOT, and 6 (26.1%) in the apex. There was a mismatch in 24 RV scars, with 22 EAS not confirmed by DCE and 2 DCE scars (both in the RVOT) undetected by EVM. In 9 (75%) of 12 patients with abnormal RV EVM/normal RV DCE, ≥1 DCEs were identified in the left ventricle (LV). Overall, ventricular DCE was detected in 78% of patients. No control subjects showed either EAS or DCE. CONCLUSIONS: EVM and CE-CMR allow identification of RV scar lesions in most ARVC patients. CE-CMR is less sensitive than EVM in identifying RV scar lesions. The high prevalence of LV DCE confirms the frequent biventricular involvement and indicates the diagnostic relevance of LV scar detection by CE-CMR.

Magnetic resonance enterography for Crohn's disease: what the surgeon can take home.

BACKGROUND: Crohn's disease (CD) is a life-long, chronic, relapsing condition requiring often morphological assessment. MR enterography (MRE) offers advantages of not using ionizing radiation and yielding intraluminal and intra-abdominal informations. The aim of our study was to identify how MRE can be useful in planning surgical procedures. PATIENTS AND METHODS: In this retrospective study, 35 patients who underwent MRE and then surgery for CD were enrolled from 2006 to 2010. MRE findings were compared to intraoperative findings. Histology of operative specimens, systemic inflammatory parameters, and fecal lactoferrin were also evaluated. Cohen's κ agreement test, sensitivity and sensibility, uni-/multivariate logistic regression, and non-parametric statistics were performed. RESULTS: MRE identified bowel stenosis with a sensitivity of 0.95 (95% CI 0.76-0.99) and a specificity of 0.72 (95% CI 0.39-0.92). The concordance of MRE findings with intraoperative findings was high [Cohen's κ = 0.72 (0.16)]. Abscesses were detected at MRE with a sensitivity of 0.92 (95% CI 0.62-0.99) and a specificity of 0.90 (95% CI 0.69-0.98) with a Cohen's κ = 0.82 (0.16). The grade of proximal bowel dilatation resulted to be a significant predictor of the possibility of using strictureplasty instead of/associated to bowel resection either at univariate or at multivariate analysis. CONCLUSION: Our study confirmed that MRE findings correlate significantly with disease activity. Detailed information about abscess could suggest percutaneous drainage that could ease the following surgery or avoid emergency laparotomy. Proximal bowel dilatation can suggest the possibility to perform bowel sparing surgery such as strictureplasty.

Clinical phenotype and diagnosis of arrhythmogenic right ventricular cardiomyopathy in pediatric patients carrying desmosomal gene mutations.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart muscle disease carrying a risk of sudden death. Information about the clinical features during childhood and the age at disease onset is scanty. OBJECTIVE: The aim of the study was to describe the ARVC phenotype as its initial clinical manifestation in a pediatric population (<18 years) with desmosomal gene mutations. METHODS: Fifty-three ARVC desmosomal gene mutation carriers (mean age 12.3 ± 3.9 years) were investigated by electrocardiogram (ECG), signal-averaged ECG, 24-hour Holter, echocardiogram, and contrast-enhanced cardiac magnetic resonance (CMR). RESULTS: None of the children ≤10 years old fulfilled the 1994 criteria, as opposed to six (33%) aged 11-14 years and eight aged >14 years (42%). At the end of follow-up (9 ± 7 years), 21 (40%) fulfilled the 1994 diagnostic criteria (mean age 16 ± 4 years). By using the 2010 criteria in subjects aged ≤18 years, 53% were unaffected, versus 62% by using the traditional criteria. More than two-thirds of affected subjects had moderate-severe forms of the disease. Contrast-enhanced CMR was performed in 21 (40%); of 13 unaffected gene mutation carriers, six showed ARVC morphological and/or tissue abnormalities. CONCLUSION: In pediatric ARVC mutation carriers, a diagnosis was achieved in 40% of cases, confirming that the disease usually develops during adolescence and young adulthood. The 2010 modified criteria seem to be more sensitive than the 1994 ones in identifying familial pediatric cases. Contrast-enhanced CMR can provide diagnostic information on gene mutation carriers not fulfilling either traditional or modified criteria. Management of asymptomatic gene mutation carriers remains the main clinical challenge.

Myocardial edema underlies dynamic T-wave inversion (Wellens' ECG pattern) in patients with reversible left ventricular dysfunction.

BACKGROUND: The Wellens' electrocardiogram (ECG) pattern of dynamic T-wave inversion in the anterior leads is observed in clinical conditions characterized by reversible left ventricular (LV) dysfunction (stunned myocardium), either ischemic or nonischemic. The pathophysiologic basis of this ECG pattern remains to be elucidated. OBJECTIVE: The purpose of this study was to report the contrast-enhanced cardiac magnetic resonance (CE-CMR) findings in 4 cases of Wellens' ECG pattern associated with transient LV dysfunction from a variety of clinical conditions such as myocardial bridge, coronary artery dissection, cholecystitis, and takotsubo syndrome. METHODS: All patients underwent CE-CMR at the time of acute clinical manifestations and after 6 to 8 weeks of follow-up to assess the presence and dynamics of LV myocardial changes. RESULTS: In all patients, the Wellens' ECG abnormalities were associated with increased signal intensity of the LV myocardium on T2-weighted sequences suggesting myocardial edema, in the absence of late enhancement on postcontrast sequences. Repolarization abnormalities and myocardial edema had a parallel time course with persistence beyond recovery of mechanical abnormalities. T-wave inversion was associated with transient prolongation of the QTc interval in all cases. CONCLUSION: The study results suggest that myocardial edema rather than systolic dysfunction underlies the Wellens' ECG pattern, regardless of the causative mechanism.

Natural time course of myocardial infarction at delayed enhancement magnetic resonance.

The case reported, who suffered prolonged coronary occlusion, was evaluated by repeated MRI images in the acute, subacute and chronic phase. Scans showed hemorrhagic myocardial infarction and massive endothelial injury and its evolution over time.

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.

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.

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).

Impact of multivessel coronary artery disease on early ischemic injury, late clinical outcome, and remodeling in patients with acute myocardial infarction treated by primary coronary angioplasty.

OBJECTIVE: The mechanism through which multivessel coronary artery disease (MVD) adversely affects the outcome of patients with ST-elevation myocardial infarction (STEMI) is poorly characterized. We assessed whether the impact of MVD on outcome of STEMI patients is because of ischemic damage after primary percutaneous coronary intervention (PPCI) or to late ischemic events. METHODS: From August 2005 to 2007, 288 STEMI patients treated by (bare metal) stent-PPCI were prospectively enrolled. The ischemic injury early after PPCI (evaluated by multiparametric approach) and the incidence of late adverse cardiovascular events were compared between the two groups. RESULTS: Compared with single vessel coronary artery disease, MVD patients (n=134) were older, with higher prevalence of diabetes, prior MI, anterior MI and higher collateral score. Myocardial perfusion as assessed by myocardial blush and SigmaST-segment resolution was similar in the two groups as well as the infarct size and microvascular obstruction as assessed by Troponin I and by the delayed enhancement of cardiac magnetic resonance. At clinical (98% complete) and echocardiogaphic (94% complete) follow-up (median 32 months) MVD patients showed a higher incidence of re-MI (6.1 vs. 1.3%), and urgent revascularization (8.3 vs. 2.7%) and worse left ventricular remodeling than single vessel disease patients. At propensity adjusted analysis MVD was an independent predictor of re-MI (odds ratio: 5.7) and ventricular remodeling (odds ratio: 2.2). CONCLUSION: The impact of MVD on clinical outcome and remodeling of STEMI patients is not because of the extent of ischemic damage observed after PPCI, but to recurrent ischemic events during follow-up.