Interatrial shunt therapy in advanced heart failure: Outcomes from the open-label cohort of the RELIEVE-HF trial.

AIMS: Heart failure (HF) outcomes remain poor despite optimal guideline-directed medical therapy (GDMT). We assessed safety, effectiveness, and transthoracic echocardiographic (TTE) outcomes during the 12 months after Ventura shunt implantation in the RELIEVE-HF open-label roll-in cohort. METHODS AND RESULTS: Eligibility required symptomatic HF despite optimal GDMT with ≥1 HF hospitalization in the prior year or elevated natriuretic peptides. The safety endpoint was device-related major adverse cardiovascular or neurological events at 30 days, compared to a prespecified performance goal. Effectiveness evaluations included the Kansas City Cardiomyopathy Questionnaire (KCCQ) at baseline, 1, 3, 6, and 12 months and TTE at baseline and 12 months. Overall, 97 patients were enrolled and implanted at 64 sites. Average age was 70 ± 11 years, 97% were in New York Heart Association class III, and half had left ventricular ejection fraction (LVEF) ≤40%. The safety endpoint was achieved (event rate 0%, p < 0.001). KCCQ overall summary score was improved by 12-16 points at all follow-up timepoints (all p < 0.004), with similar outcomes in patients with reduced and preserved LVEF. At 12 months, left ventricular end-systolic and end-diastolic volumes were reduced (p = 0.020 and p = 0.038, respectively), LVEF improved (p = 0.009), right ventricular end-systolic and end-diastolic areas were reduced (p = 0.001 and p = 0.030, respectively), and right ventricular fractional area change (p < 0.001) and tricuspid annular plane systolic excursion (p < 0.001) improved. CONCLUSION: Interatrial shunting with the Ventura device was safe and resulted in favourable clinical effects in patients with HF, regardless of LVEF. Improvements of left and right ventricular structure and function were consistent with reverse myocardial remodelling. These results would support the potential of this shunt device as a treatment for HF.

A prospective study on myocardial injury after BNT162b2 mRNA COVID-19 fourth dose vaccination in healthy persons.

AIMS: To prospectively evaluate the incidence of myocardial injury after the administration of the fourth dose BNT162b2 mRNA vaccine (Pfizer-BioNTech) against COVID-19. METHODS AND RESULTS: Health care workers who received the BNT162b2 vaccine during the fourth dose campaign had blood samples collected for high-sensitivity cardiac troponin (hs-cTn) during vaccine administration and 2-4 days afterward. Vaccine-related myocardial injury was defined as hs-cTn elevation above the 99th percentile upper reference limit and >50% increase from baseline measurement. Participants with evidence of myocardial injury underwent assessment for possible myocarditis. Of 324 participants, 192 (59.2%) were female and the mean age was 51.8 ± 15.0 years. Twenty-one (6.5%) participants had prior COVID-19 infection, the mean number of prior vaccine doses was 2.9 ± 0.4, and the median time from the last dose was 147 (142-157) days. Reported vaccine-related adverse reactions included local pain at injection site in 57 (17.59%), fatigue in 39 (12.04%), myalgia in 32 (9.88%), sore throat in 21 (6.48%), headache in 18 (5.5%), fever ≥38°C in 16 (4.94%), chest pain in 12 (3.7%), palpitations in 7 (2.16%), and shortness of breath in one (0.3%) participant. Vaccine-related myocardial injury was demonstrated in two (0.62%) participants, one had mild symptoms and one was asymptomatic; both had a normal electrocardiogram and echocardiography. CONCLUSION: In a prospective investigation, an increase in serum troponin levels was documented among 0.62% of healthy health care workers receiving the fourth dose BNT162b2 vaccine. The two cases had mild or no symptoms and no clinical sequela. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT05308680.

Apixaban vs. warfarin in patients with left ventricular thrombus: a prospective multicentre randomized clinical trial‡.

AIMS: Current guidelines recommend anticoagulation with a vitamin K antagonist to treat left ventricular (LV) thrombus after myocardial infarction (MI). Data on the use of direct oral anticoagulants (DOACs) in this setting are limited. The aim of the study was to assess the efficacy of apixaban vs. warfarin in treating LV thrombus after MI. METHODS AND RESULTS: We conducted a prospective, randomized, multicentre open-label clinical trial including patients with LV thrombus detected by 2D transthoracic echocardiography 1-14 days after acute MI. Thirty-five patients were enrolled in three medical centres; 17 patients were randomized to warfarin and 18 patients to apixaban. The primary outcome was the presence and size of LV thrombus 3 months after initiation of anticoagulation. Secondary outcomes were major bleeding, stroke or systemic embolism, re-hospitalization, and all-cause mortality. Mean LV thrombus size at enrolment was 18.5 mm × 12.3 mm in the warfarin group and 19.9 mm × 12.4 mm in the apixaban group (P = NS). Thirty-two patients completed 3 months follow-up. In the warfarin group, two patients withdrew, and in the apixaban group one patient died. Thrombus completely resolved in 14 of 15 patients in the warfarin group and in 16 of 17 patients in the apixaban group (P = NS and P = 0.026 for non-inferiority). Two patients had major bleeding in the warfarin group, while no major bleeding events were recorded in the apixaban group. There was one stroke in the warfarin group and one death in the apixaban group. CONCLUSION: Our results suggest that apixaban is non-inferior to warfarin for treatment of patients with LV thrombus after acute MI with a 20% non-inferiority margin.

Disparities in the characteristics and outcomes of patients hospitalized with acute decompensated heart failure admitted to internal medicine and cardiology departments: a single-centre, retrospective cohort study.

AIMS: Efforts are constantly made to decrease the rates of readmission after acute decompensated heart failure (ADHF). ADHF admissions to internal medicine departments (IMD) were previously associated with higher risk for readmission compared with those admitted to cardiology departments (CD). It is unknown if the earlier still applies after recent advancement in care over the last decade. This contemporary cohort compares characteristics and outcomes of ADHF patients admitted to IMD with those admitted to CD. METHODS AND RESULTS: The data for this single-centre, retrospective study utilized a cohort of 8332 ADHF patients admitted between 2007 and 2017. We compared patients' baseline characteristics and clinical and laboratory indices of patients admitted to CD and IMD with the outcome defined as 30 day readmission rate. In comparison with those admitted to CD, patients admitted to IMD (89.5% of patients) were older (79 [70-86] vs. 69 [60-78] years; P < 0.001) and had a higher incidence of co-morbidities and a higher ejection fraction. Readmission rates at 30 days were significantly lower in patients admitted to CD (15.9% vs. 19.6%; P = 0.01). Conflicting results of three statistical models failed to associate between the admitting department and 30 day readmission (odds ratio for 30 day readmission in CD: forced and backward stepwise logistic regression 0.8, 95% confidence interval 0.65-0.97, P = 0.02; stabilized inverse probability weights model odds ratio 1.0, confidence interval 0.75-1.37, P = 0.96). CONCLUSIONS: This contemporary analysis of ADHF patient cohort demonstrates significant differences in the characteristics and outcomes of patients admitted to IMD and CD. Thus, focusing strategies for readmission prevention in patients admitted to IMD may be beneficial.

Left atrial remodeling postseptal myectomy for severe obstructive hypertrophic cardiomyopathy: Analysis by two-dimensional speckle-tracking echocardiography.

BACKGROUND: Septal myectomy relieves left ventricular outflow obstruction (LVOTO) and is associated with excellent long-term outcomes. LVOTO is associated with diastolic dysfunction and increased left atrial (LA) size. We sought to investigate the changes in LA volumes and function postmyectomy and the association between these changes with clinical outcomes postmyectomy. METHODS: Sixty-six hypertrophic cardiomyopathy patients undergoing myectomy were retrospectively studied. Preprocedural and 6- to 18-month postmyectomy follow-up transthoracic echocardiographic images were obtained. LA volumes and strain were assessed by two-dimensional speckle-tracking echocardiography. RESULTS: Left atrial volumes, that is, indexed maximal, minimal, and pre-A volumes reduced postmyectomy, yet remained increased compared to controls (105.6 ± 34.5 mL vs 84.9 ± 26.7 mL, 45.2 ± 25.7 mL vs 35.4 ± 22.6 mL, 70.1 ± 31.4 mL vs 35.4 ± 22.6 mL, respectively, P < 0.05). The total emptying index did not improve postmyectomy and remained lower than controls (58.6 ± 12.4 vs 59.9 ± 12.8, P = NS) whereas atrial contraction improved, yet did not normalize (active emptying index 36.1 ± 14.9 vs 41.1 ± 16.2, P < 0.05). The conduit volume remained reduced postmyectomy (18.6 ± 13.3 mL vs 16.6 ± 15.1 mL, P = NS). LA strain also did not improve postmyectomy (26.8 ± 7.3 vs 28.5 ± 8.8, P = NS). A multivariable logistic regression identified preprocedural E/e' ratio and indexed maximal LA volume, as independent predictors for LA volume reduction ≥20% postmyectomy. During a mean follow-up of 4.9 ± 2.3 years postmyectomy, 24.2% of the patients developed atrial fibrillation and <5% of patients were severely symptomatic. We found no associations between LA volumes/function and atrial fibrillation or symptoms postmyectomy. CONCLUSION: Postmyectomy LA volumes decreased, and the contractile function improved. There was no association between LA volumes/function and clinical outcomes postmyectomy. Notably, the LA remained enlarged (though to a lesser degree) with reduced strain and emptying fraction, suggesting possible atrial myopathy.

Speckle tracking imaging in inflammatory heart diseases.

Accurate diagnosis of acute myocarditis is important for the prognosis and risk stratification of these patients. Cardiac magnetic resonance (CMR) has become a major modality for diagnosis of myocarditis, but not widely available. In this study, we tried to evaluate regional and global longitudinal strain by speckle tracking echocardiography in patients with acute inflammatory myocardial diseases in correlation with CMR. Patients with suspected acute myocarditis were recruited prospectively. Clinical diagnosis was established based on clinical, electrocardiographic, laboratory and conventional echocardiographic data. All patients underwent CMR and repeat echocardiographic examination within 24 h of CMR. Echocardiographic examinations were analyzed offline with speckle tracking imaging software. Thirty-two patients with acute perimyocarditis and myopericarditis were included. Mean age was 29 ± 8, 30 males. All patients presented with chest pain and an abnormal electrocardiogram, in 28 ST elevation was found. Troponin was elevated in 30 and was 0.7 ± 0.5 ng/ml. Creatine kinase was 487 ± 319 U. LVEF was 56 ± 5%. Wall motion abnormalities were present in postero-lateral (53%), and inferior wall (21%). Delayed enhancement on CMR was found in 29 patients. Echocardiographic EF based on speckle tracking imaging correlated with CMR calculated EF. There was a positive correlation between the amplitude of regional strain and delayed enhancement, r = 0.52. Sensitivity and specificity of regional strain for prediction of delayed enhancement was 85 and 73% respectively. Speckle tracking imaging can help in the diagnosis of acute myocarditis when CMR is not readily available. Speckle tracking imaging based EF correlates with CMR calculated LVEF and with global strain.

[ONE YEAR FOLLOW-UP OF PATIENTS AFTER CARDIAC ARREST TREATED WITH THERAPEUTIC HYPOTHERMIA: PROSPECTIVE COHORT STUDY COMPARED WITH HISTORICAL CONTROL].

BACKGROUND: Mild therapeutic hypothermia has been shown to reduce mortality and neurological morbidity in post cardiac arrest survivors. These beneficial effects had initially been reported in retrospective studies and subsequently more evidence has been gathered by two cornerstone randomized control trials. All these studies focused on the acute outcome and the clinical status at the time of hospital discharge. The main goal of this study was to describe the long term effects of therapeutic hypothermia in this population. PATIENTS AND METHODS: A prospective cohort with a historical control group was used in this study. All consecutive patients eligible for therapeutic hypothermia after cardiac arrest were enrolled. These patients were compared to an historical control group of patients who had met the same criteria of treatment with therapeutic hypothermia, but were not treated since it was not yet available. Patients' records and clinical assessment at 1 week, one, six and twelve months follow-up were collected. RESULTS: In the present study 54 consecutive patients were recruited prospectively, treated with mild hypothermia and 41 patients served as the historical control group for a similar period of time. The cooling group was significantly younger than the control group, 54 ± 16.3 versus 61.1 ± 14.5 years (p < 0.04). Peripheral arterial embolism complication was more common in the hypothermia group. 11.1% versus 0% (p < 0.035). No other clinically meaningful differences were found. In this respect, the beneficial trend towards reduced neurological outcome and mortality was observed in favor of the cooling group, which was statistically significant at six months follow-up (p < 0.044). Beyond 6 months the differences did not reach statistical significance. CONCLUSION: In the current phase of the study, a tendency in favor of mild cooling was observed in the short and medium term outcomes in patients resuscitated after out of hospital cardiac arrest due to fatal arrhythmia. The current results indicate that in spite of high survival rates after the acute stage in the cooling group, the long term mortality rate in this group is still high.

Myocardial mechanical remodeling after septal myectomy for severe obstructive hypertrophic cardiomyopathy.

BACKGROUND: Septal myectomy for symptomatic patients with hypertrophic obstructive cardiomyopathy (HOCM) is a well-established procedure for symptomatic relief. Myocardial mechanics are abnormal in patients with HOCM, demonstrating low longitudinal strain, high circumferential strain, and high apical rotation compared with healthy subjects. The aim of this study was to determine whether functional improvement after myectomy is associated with improved myocardial mechanics. METHODS: Clinical data and paired echocardiographic studies before and after myectomy (6-18 months) were retrospectively analyzed and compared in 66 patients (mean age, 54 ± 13 years; 64% men) with HOCM. Myocardial mechanics including longitudinal and circumferential strain and rotation were assessed using two-dimensional strain software (Velocity Vector Imaging). RESULTS: Patients had significant symptomatic alleviation (mean New York Heart Association class, 2.8 ± 0.4 at baseline and 1.3 ± 0.5 after myectomy; P < .05). Left ventricular outflow gradient decreased dramatically (from 93 ± 26 to 17 ± 12 mm Hg; P < .05), and left atrial volume index decreased (from 48 ± 16 to 37 ± 13 cm(3)/m(2); P < .05). Low longitudinal strain decreased at the myectomy site, increased in the lateral segments, and remained unchanged globally (-16 ± 4). High circumferential strain decreased (from -31 ± 5 to -25 ± 6, P < .05). High left ventricular twist normalized (from -15.5 ± 6.2° to 12.8 ± 4.2°, P < .05). Independent predictors of symptomatic response included younger age before myectomy, thinner posterior wall, and higher lateral early diastolic velocity (e'). CONCLUSION: In patients with HOCM, surgical myectomy alleviated symptoms, relieved obstruction, and decreased left atrial volume index. Longitudinal strain remained unchanged, but circumferential strain and rotation decreased, demonstrating different mechanical adaptations to chronic elevated afterload seen in patients with severe aortic stenosis undergoing valve replacement. Disease extent (age, posterior wall involvement) and the presence of diastolic dysfunction seem to be related to partial symptomatic response to myectomy.

Myocardial fibrosis in hypertrophic cardiomyopathy: accurate reflection of histopathological findings by CMR.

OBJECTIVES: In this study we sought to explore the relationship between cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) and histopathological parameters including interstitial fibrosis and replacement fibrosis (scar) in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: CMR-LGE is a well-established tool for the assessment of scar in ischemic heart disease. Its role in HCM has evolved in recent years, and an association with nonsustained ventricular tachycardia has been demonstrated. METHODS: HCM patients who underwent septal myectomy during the period 2004 through 2010 and had undergone CMR-LGE no more than 6 months before surgery were selected. Histopathological assessment of the myectomy specimens included quantitative digital analysis (interstitial and replacement fibrosis) and semiquantitative assessment (small intramural coronary arteriole dysplasia and disarray). Correlations between CMR-LGE measured with various techniques, SD above the signal intensity for the normal remote myocardium (2, 4, 5, 6, and 10 SD) and the full width at half maximum (FWHM) technique, at the myectomy site, and interstitial fibrosis, replacement fibrosis (scar), and their sum (fibrosis + scar) were evaluated. RESULTS: Twenty-nine patients were included. Statistically significant correlations between CMR-LGE (at 2, 4, 5, 6, 10 SD and by the FWHM technique), and both interstitial fibrosis and the combined interstitial and replacement fibrosis were found. The strongest correlation was between combined interstitial and replacement fibrosis and CMR-LGE measured at 5 SD (r = 0.78, p < 0.0001). LGE measured at 10 SD demonstrated the best correlation with replacement fibrosis (r = 0.42, p = 0.02). Bland-Altman analysis revealed optimum agreement between the combined interstitial and replacement fibrosis found at pathology and LGE measured at 4 SD. In addition, moderate and severe small intramural coronary artery dysplasia showed a statistically significant correlation with replacement fibrosis (p = 0.01) and CMR-LGE at 10 SD (p = 0.04). CONCLUSIONS: CMR-LGE measured at 4 SD and 5 SD yields the closest approximation to the extent of total fibrosis measured by the histopathological standard of reference. These findings have implications for future investigations of CMR-LGE and its association with important clinical endpoints in HCM, including sudden cardiac death.

Toronto hypertrophic cardiomyopathy genotype score for prediction of a positive genotype in hypertrophic cardiomyopathy.

BACKGROUND: Genotyping in hypertrophic cardiomyopathy has gained increasing attention in the past decade. Its major role is for family screening and rarely influences decision-making processes in any individual patient. It is associated with substantial costs, and cost-effectiveness can only be achieved in the presence of high-detection rates for disease-causing sarcomere protein gene mutations. Therefore, our aim was to develop a score based on clinical and echocardiographic variables that allows prediction of the probability of a positive genotype. METHODS AND RESULTS: Clinical and echocardiographic variables were collected in 471 consecutive patients undergoing genetic testing at a tertiary referral center between July 2005 and November 2010. Logistic regression for a positive genotype was used to construct integer risk weights for each independent predictor variable. These were summed for each patient to create the Toronto hypertrophic cardiomyopathy genotype score. A positive genotype was found in 163 of 471 patients (35%). Independent predictors with associated-risk weights in parentheses were as follows: age at diagnosis 20 to 29 (-1), 30 to 39 (-2), 40 to 49 (-3), 50 to 59 (-4), 60 to 69 (-5), 70 to 79 (-6), ≥80 (-7); female sex (4); arterial hypertension (-4); positive family history for hypertrophic cardiomyopathy (6); morphology category (5); ratio of maximal wall thickness:posterior wall thickness <1.46 (0), 1.47 to 1.70 (1), 1.71 to 1.92 (2), 1.93 to 2.26 (3), ≥2.27 (4). The model had a receiver operator curve of 0.80 and Hosmer-Lemeshow goodness-of-fit P=0.22. CONCLUSIONS: The Toronto genotype score is an accurate tool to predict a positive genotype in a hypertrophic cardiomyopathy cohort at a tertiary referral center.

Impact of frequent nocturnal hemodialysis on myocardial mechanics and cardiomyocyte gene expression.

BACKGROUND: Regression of left ventricular mass with nocturnal hemodialysis has been observed. The influence of nocturnal hemodialysis on myocardial mechanics and cardiomyocyte gene expression is unknown. METHODS AND RESULTS: Forty-two patients (30 male:12 female; age, 44 ± 12 years [mean ± SD]) with end-stage renal disease were followed for 3.1 ± 1.8 years before and after conversion to nocturnal hemodialysis and were compared with 29 normal subjects (18 male:11 female; age, 48 ± 13 years). Myocardial mechanics were assessed by 2-dimensional velocity vector imaging. Uremic plasma (10%) was added to cultures of neonatal Sprague-Dawley rat ventricular myocytes. Total RNA was isolated from cell cultures and subjected to differential gene expression profiling with specific interest in genes affecting apoptosis and fibrosis. Left ventricular mass index and left atrial volume index decreased from 122.6 ± 42.6 to 98.5 ± 34.9 g/m(2) (P<0.001) and 25.9 ± 9.1 to 22.5 ± 9.6 cm(3)/m(2) (P=0.005), respectively. Left ventricular apical circumferential strain and basal rotation improved after conversion to nocturnal hemodialysis and approximated normal values. Nocturnal hemodialysis increased sessional dialysis dose and lowered parathyroid hormone levels (from 51 ± 67 to 24 ± 37 pmol/L, P<0.05) and phosphate. Under conventional hemodialysis conditions, there was an upregulation of genes leading to apoptosis and fibrosis in cardiomyocytes. The change in left ventricle rotation was associated with the change in parathyroid hormone values (r=0.37, P=0.02) and to the change in left ventricle mass (r=0.31, P=0.046). CONCLUSIONS: Frequent hemodialysis is associated with improvement in myocardial mechanics and cardiac gene expression profile, which warrants prognostic validation.

Speckle tracking imaging in acute inflammatory pericardial diseases.

BACKGROUND: Left ventricular (LV) function in acute perimyocarditis is variable. We evaluated LV function in patients with acute perimyocarditis with speckle tracking. METHODS: Thirty-eight patients with acute perimyocarditis and 20 normal subjects underwent echocardiographic examination. Three-layers strain and twist angle were assessed with a speckle tracking. Follow-up echo was available in 21 patients. RESULTS: Strain was higher in normal subjects than in patients with perimyocarditis. Twist angle was reduced in perimyocarditis--10.9° ± 5.4 versus 17.6° ± 5.8, P < 0.001. Longitudinal strain and twist angle were higher in normal subjects than in patients with perimyocarditis and apparently normal LV function. Follow-up echo in 21 patients revealed improvement in longitudinal strain. CONCLUSIONS: Patients with acute perimyocarditis have lower twist angle, longitudinal and circumferential strain. Patients with perimyocarditis and normal function have lower longitudinal strain and twist angle. Short-term follow-up demonstrated improvement in clinical parameters and longitudinal strain despite of residual regional LV dysfunction.

Sarcomere protein gene mutations in patients with apical hypertrophic cardiomyopathy.

BACKGROUND: Apical hypertrophic cardiomyopathy (HCM) is a unique form of HCM with left ventricular hypertrophy confined to the cardiac apex. The purpose of our study was to report genetic findings in a large series of unrelated patients with apical HCM and compare them with a nonapical HCM cohort. METHODS AND RESULTS: Overall, 429 patients with HCM underwent genetic testing. The panel included 8 sarcomere protein genes and 3 other genes (GLA, PRKAG2, and LAMP2). Sixty-one patients were diagnosed with apical HCM. A positive genotype was found in 8 patients with apical HCM. The genotype-positive and genotype-negative patients had similar maximal wall thicknesses (17.5 ± 3.5 mm versus 17.6 ± 3.3 mm, P = 0.71) and similar frequency of HCM-related events (2/8; 25% versus 13/53; 25%; P = 0.98). Thirteen percent with apical HCM and 40% with nonapical HCM had a positive genotype (P<0.001) most often involving the MYBPC3 and MYH7 genes. CONCLUSIONS: In apical HCM, a positive genotype was found less frequently than in nonapical HCM, and it was most often involving MYBPC3 and MYH7 genes. Only 13% of patients with apical HCM were found to be genotype positive, indicating that genome-wide association studies and gene expression profiling are needed for better understanding of the genetic background of the disease. There was no significant genotype-phenotype correlation in our cohort with apical HCM.

Can dobutamine stress echocardiography induce cardiac troponin elevation?

BACKGROUND: Elevation of cardiac troponin (cTn) is considered specific for myocardial damage. Elevated cTn and echocardiogrpahic documentation of wall motion abnormalities (WMAs) that were recorded after extreme physical effort raise the question whether dobutamine stress echo (DSE), can also induce elevation of troponin. METHODS: we prospective enrolled stable patients (age >18 years) referred to DSE. The exam was performed under standardized conditions. Blood samples for cTnI were obtained at baseline and 18-24 hours after the test. We aimed to compare between the clinical and echocardiographic features of patients with elevated cTnI and those without cTnI elevations. RESULTS: Fifty-seven consecutive patients were included. The average age was 64.4 ± 10.7, 73% of the patients were males, and nearly half of the patients were known to have ischemic heart disease. Two of the patients were excluded due to technical difficulty. No signs of ischemia were recorded in 25 (45.4%). Among the patients with established ischemia on DSE, 12 (22%) had mild ischemia, 13 (23.6%) had moderate and 5 (9%) had severe ischemia. Angiography was performed in 13 (26%) of the patients, of which 7 had PCI and one was referred to bypass surgery. None of the patients had elevated cTnI 18-24 hours after the DSE. CONCLUSIONS: Our results indicate that there is no elevation of cTn despite the occurrence of significant WMAs on DSE. We conclude that cTnI cannot be used as an additional diagnostic tool during pharmacological stress test performed to evaluate the presence and severity of ischemia.

Intracoronary administration of autologous bone marrow mononuclear cells in patients with chronic ischemic symptomatic cardiomyopathy: 5 years follow-up.

BACKGROUND: Several studies have demonstrated the shortterm safety, feasibility and efficacy of cell transplantation in patients with advanced heart failure. Data on the long-term outcome are lacking. OBJECTIVES: To evaluate the long-term outcome of intracoronary autologous bone marrow administration in patients with stable severe ischemic cardiomyopathy who were not suitable for revascularization. METHODS: We enrolled eight consecutive patients with ischemic cardiomyopathy: all were in NYHA functional class III-IV despite optimal medical treatment. Dobutamine stress echo showed that all had left ventricular ejection fraction < 35% with significant viability or ischemia, or both, in at least two myocardial segments. Based on coronary anatomy none of the patients was suitable for revascularization. Bone marrow was obtained and the cells were injected into all patent conduits after a brief balloon occlusion at a normal coronary segment. Clinical followup was performed periodically at the heart failure clinic, and included electrocardiography, laboratory tests and echocardiography. RESULTS: During 5 years follow-up there were two deaths: one due to leukocytoclastic vasculitis 21 months after intracoronary bone marrow infusion, and the second patient died suddenly during sleep 30 months after the transplant. The other six patients are alive, two of them without any cardiovascular or clinical events. No significant change in systolic and diastolic function was observed on echocardiography. CONCLUSIONS: Despite the small and selected patient group, our long-term follow-up showed a promising outcome for this population of patients suffering from severe cardiac disease. Longer follow-up of a much larger group is needed.

Acute myocardial infarction with spontaneous reperfusion: clinical characteristics and optimal timing for revascularization.

BACKGROUND: Spontaneous coronary reperfusion occurs in 7-27% of patients with ST elevation myocardial infarction, and is an independent predictor of myocardial salvage, percutaneous coronary intervention success, and improved outcome. OBJECTIVES: To determine the optimal PCI time for patients admitted to the hospital due to STEMI with SCR. METHODS: We performed a retrospective analysis of all patients admitted to the coronary care unit between July 2002 and November 2004 with a diagnosis of STEMI with SCR. RESULTS: The study group comprised 86 patients. There was not a single reinfarction episode during an observation period of 6579 patient hours. Cardiac catheterization was executed early (< 24 hours from pain onset) in 26 patients and late (> 24 hours) in 55. Pre-PCI angiographic TIMI flow 2-3 was seen in > 95% in both groups. PCI was performed more frequently in the "early" group (P = 0.024), while multi-vessel coronary artery disease (P = 0.094) requiring coronary bypass surgery (P = 0.056) was observed more frequently in the "late catheterization" group. Myocardial infarction and angina pectoris at 30 days occurred more frequently in the early catheterization group (P = 0.039), however no difference in any major adverse cardiac events was detected during long-term follow-up (491 +/- 245 days). CONCLUSIONS: Reinfarction after STEMI with SCR is a rare event. Early PCI in patients with STEMI and SCR, even when executed with aggressive antiplatelet therapy, seems to result in an excess of early MACE without any long-term advantage. Prospective randomized trials should determine the optimal PCI timing for these patients.

[ST myocardial infarction with spontaneous coronary reperfusion].

ST elevation myocardial infarction continues to be a major medical problem even in the beginning of the 21st century. Treatment guidelines for these patients are based on multiple randomized clinical trials. In order to minimize myocardial damage, early patency of the infarct relating artery must be accomplished. This is the major difference in the treatment strategy between ST elevation myocardial infarction and other acute coronary syndromes. Primary percutaneous coronary intervention and fibrinolysis are the two treatment modalities for achieving myocardial reperfusion. The subgroup of ST elevation myocardial infarction with spontaneous coronary artery reperfusion carries a more favorable prognosis. This review addresses the clinical characteristics, natural history, prognosis and treatment strategies for this group, with special emphasis on the optimal timing for revascularization, and the role of glycoprotein IIb/IIIa inhibitors.