19 research outputs found

    Effect of aliskiren on post-discharge outcomes among diabetic and non-diabetic patients hospitalized for heart failure: insights from the ASTRONAUT trial

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    Aims The objective of the Aliskiren Trial on Acute Heart Failure Outcomes (ASTRONAUT) was to determine whether aliskiren, a direct renin inhibitor, would improve post-discharge outcomes in patients with hospitalization for heart failure (HHF) with reduced ejection fraction. Pre-specified subgroup analyses suggested potential heterogeneity in post-discharge outcomes with aliskiren in patients with and without baseline diabetes mellitus (DM). Methods and results ASTRONAUT included 953 patients without DM (aliskiren 489; placebo 464) and 662 patients with DM (aliskiren 319; placebo 343) (as reported by study investigators). Study endpoints included the first occurrence of cardiovascular death or HHF within 6 and 12 months, all-cause death within 6 and 12 months, and change from baseline in N-terminal pro-B-type natriuretic peptide (NT-proBNP) at 1, 6, and 12 months. Data regarding risk of hyperkalaemia, renal impairment, and hypotension, and changes in additional serum biomarkers were collected. The effect of aliskiren on cardiovascular death or HHF within 6 months (primary endpoint) did not significantly differ by baseline DM status (P = 0.08 for interaction), but reached statistical significance at 12 months (non-DM: HR: 0.80, 95% CI: 0.64-0.99; DM: HR: 1.16, 95% CI: 0.91-1.47; P = 0.03 for interaction). Risk of 12-month all-cause death with aliskiren significantly differed by the presence of baseline DM (non-DM: HR: 0.69, 95% CI: 0.50-0.94; DM: HR: 1.64, 95% CI: 1.15-2.33; P < 0.01 for interaction). Among non-diabetics, aliskiren significantly reduced NT-proBNP through 6 months and plasma troponin I and aldosterone through 12 months, as compared to placebo. Among diabetic patients, aliskiren reduced plasma troponin I and aldosterone relative to placebo through 1 month only. There was a trend towards differing risk of post-baseline potassium ≥6 mmol/L with aliskiren by underlying DM status (non-DM: HR: 1.17, 95% CI: 0.71-1.93; DM: HR: 2.39, 95% CI: 1.30-4.42; P = 0.07 for interaction). Conclusion This pre-specified subgroup analysis from the ASTRONAUT trial generates the hypothesis that the addition of aliskiren to standard HHF therapy in non-diabetic patients is generally well-tolerated and improves post-discharge outcomes and biomarker profiles. In contrast, diabetic patients receiving aliskiren appear to have worse post-discharge outcomes. Future prospective investigations are needed to confirm potential benefits of renin inhibition in a large cohort of HHF patients without D

    Incidence of Coronary Embolism in Group of Patients with Atrial Fibrillation and Myocardial Infarction

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    Embolic myocardial infarction (EMI) is more common than gets to be diagnosed. EMI is often associated with atrial fibrillation (AF). The incidence of this pathology, prognosis and treatment tactics remain unclear.&#x0D; AIM: To assess the incidence of EMI among patients with myocardial infarction (MI), genesis of coronary embolism (CE), initial characteristics, treatment and prognosis in group of patients with EMI.&#x0D; MATERIALS AND METHODS: The group of patients with EMI was selected among 1989 patients with MI admitted to the cardiology department of the North-Western State Medical University named after I.I. Mechnikov between 2013 to December 2019. The CE verification criteria were the SUITA criteria. Statistical data processing was carried out using the SAS program.&#x0D; RESULTS: 16 cases of EMI were registered (0.8% of all MI and 4.3% of patients with MI and AF). 68.7% (95% CI = 41.5%88.9%) of patients with EMI had AF. All patients with EMI and AF did not have adequate anticoagulant therapy before admission. Among patients with EMI, men predominated, they were younger, had fewer comorbidities than patients with MI and without AF. 13 of 16 patients with EMI were prescribed anticoagulants. During hospitalization, the composite endpoint (pulmonary embolism + stroke + cardiovascular death) was recorded in 25% (95% CI = 7.3%52.2%), in the long-term period in 30% of cases (95 % CI = 6.765.2). All these patients had AF. EMI in patients with AF was associated with the development of severe chronic heart failure (CHF) by the time of discharge and with decompensation of CHF in the long-term period.&#x0D; CONCLUSIONS: EMI often occur in group of patients with AF, always in the absence of adequate anticoagulant therapy. Patients with EMI and AF have a worse prognosis due to recurrent thromboembolic events.&#x0D; Keywords: anticoagulants; atrial fibrillation; coronary embolism; embolic myocardial infarction; prognosis; thrombaspiration.</jats:p

    Antithrombotic therapy and its impact on prognosis in patients with atrial fibrillation and myocardial infarction. Long-term observation results

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    Aim. To study antithrombotic therapy (ATT) in patients with myocardial infarction (MI) type 1 and preexisting atrial fibrillation (AF), effect of ATT on prognosis.&#x0D; Material and methods. 100 patients with type 1 MI and preexisting AF were selected. The exclusion criterion was severe concomitant pathology.&#x0D; Results. Only 13.0% of AF patients took anticoagulants (AC) adequately before hospitalization. 94.0% of patients in hospital and 80.5% at discharge were prescribed triple ATT at least for 1 month with transition to dual ATT (AC + disaggregant) for 12 months. ACs were prescribed in hospital in 100.0% of cases, at discharge in 93.1%. After 1 year 8.4% of patients stopped taking ACs, after 2.31.9 years 15.7%. The incidence of ischemic and hemorrhagic events didnt differ in patients with different regimens of ATT (double/triple) and types of AСs (vitamin K antagonists/non-vitamin K antagonist ACs). In the long-term period patients, who took ACs incorrectly or stopped taking ACs, had increased risks of stroke (OR 9.580; 95% CI 1.15379.599, p=0.0365); combined endpoint: recurrent MI + stroke + cardiovascular mortality (OR 2.556; 95% CI 1.1045.918, p=0.0284).&#x0D; Сonclusion. Patients with preexisting AF had a low adherence to ACs prior to MI. It increased after hospitalization and decreased during follow-up. In the long-term period patients, who took ACs incorrectly or stopped taking ACs, had significantly increased risks of stroke, combined endpoint. There were no differences in the prognosis depending on the type of ACs, the regimens of ATT administered in accordance with ischemic and hemorrhagic risks.</jats:p

    Characteristics of clinical signs, laboratory and instrumental examinations in various mechanisms of development of type 2 myocardial infarction

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    Aim. To identify different pathogenetic variants of myocardial infarction type 2 (MI-2).&#x0D; Material and methods. Reviewed 4168 cases of MI admitted in multidisciplinary hospital for 10 years. 353 patients met the criteria for MI-2 without signs of coronary atherothrombosis (CA). In the study group, the features of clinical and laboratory-instrumental manifestations were evaluated.&#x0D; Results. Cases of IM-2 were subdivided into 4 clinical-pathogenic variants (CPV): 1-CPV developed due an increasing in myocardial oxygen demand; 2-CPV, arising from a decrease in the supply of oxygen; 3-CPV associated with local coronary circulation disorder; 4-CPV developed due to the combined oxygen-energy imbalance. In 72 (20.4%) cases, 1-CPV was detected, caused by a hypertensive crisis and/or tachyarrhythmias; 2-CPV observed in 73 (20.68%) patients with hypotension, anemia, microvascular dysfunction, respiratory failure; 3-CPV caused by spasm and embolism of CA was detected in 47 (13.31%) cases; in 161 (45.61%) patients, IM-2 is associated with increased myocardial oxygen demand with reduced oxygen delivery. The gender and risk factors in groups are comparable. The average age of 1-CPV- and 3-CPV-patients was less and amounted to 65.7 and 56.5 versus 70.2 and 73.8 years in the 2-CPV and 4-CPV. Typical clinical and laboratory-instrumental signs of MI were common for patients with 1-CPV and 3-CPV, while 2-CPV and 4-CPV more often had chronic severe pathology, multivessel coronary disorder, and the clinical presentation and ischemic signs were less common.&#x0D; Conclusion. Clinical manifestations and results of examination of patients with MI-2 depend on the mechanism of its development.</jats:p

    Myocardial infarction type 2 and myocardial injury: The current state of the problem

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    Today, the most difficult in terms of diagnosis and treatment today among various types of myocardial infarction (MI) is MI type 2 (MI-2). The lack of clinical guidelines for management of patients with this type of MI, as well as the literature data on prevalence, patient characteristics and prognosis contributes to the scientific relevance of the further research.</jats:p

    Spontaneous coronary artery dissection in a young woman with signs of connective tissue dysplasia and hereditary thrombophilia: clinical case

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    BACKGROUND: Spontaneous coronary artery dissection (SCAD) is a disease that develops unrelated to intracoronary intervention, atherosclerosis, aortic dissection, or mechanical trauma and causes a false lumen (intramural hematoma) in the wall of the coronary artery (CA) with impaired blood flow in it and myocardial ischemia in the affected region of the CA. SCAD most often develops in young and middle-aged adults (aged ≤50 years); among women, it becomes the culprit in 24%–35% of cases of acute myocardial infarction (MI). SCAD is a risk factor for MI, and incorrect interpretation of the angiographic picture and intravascular imaging methods can lead to incorrect tactics of patient behavior. CLINICAL CASE DESCRIPTION: This article presents a clinical case of SCAD leading to the development of MI in a young woman with concomitant connective tissue dysplasia and hereditary thrombophilia. The angiographic disease course resembled focal atherosclerosis, and in the course of invasive management, complications had arisen, confirming the probable genesis of coronary artery obstruction. CONCLUSION: SCAD is a complex disease, with a sudden onset and an ambiguous prognosis. In most cases, SCAD develops in young women in the absence of cardiovascular factors. It is difficult to diagnose because its signs and symptoms are similar to more common diseases, mainly MI. SCAD can masquerade as focal stenosis on an angiogram, mimicking an atherosclerotic plaque. The «gold standard» for diagnosing SCAD is optical coherence tomography (OCT). OCT enables the visualization of the state of all coronary artery walls and elucidates the pathogenetic mechanisms of MI. If performing OCT is impossible after diagnostic coronary angiography in young patients in suspected cases, the likelihood of DST and SCAD risk must be assessed to avoid errors in choosing treatments. The technical accessibility of intracoronary imaging methods reduces the frequency of diagnostic and, consequently, treatment errors

    A clinical case of takotsubo syndrome in combination with left ventricular hypertrabeculation

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    The article describes the clinical case of takotsubo syndrome in female, who has also echocardiographic picture of a left ventricular noncompaction cardiomyopathy. According to the result of magnetic resonance imaging, the diagnosis of noncompaction cardiomyopathy was not confirmed, left ventricular hypertrabeculation was revealed. There are single descriptions of the combination of takotsubo syndrome and left ventricular hypertrabeculation, the pathogenetic relationship of these conditions has not yet been established.</jats:p

    Prediction of in-hospital complications in takotsubo syndrome: prospective cohort study

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    BACKGROUND: Until recently, takotsubo syndrome (TS) was considered a fairly benign disease in both early and late periods. However, in recent years, in-hospital complications in the acute period of TS are common and can be life-threatening. AIM: Based on clinical and laboratory-instrumental data, this study aimed to build models for predicting the risk of developing in-hospital complications in patients with TS during the acute period. MATERIALS AND METHODS: This prospective cohort study included 60 patients with TS, with an average age of 65.5±13.4 years. In the acute period (7–14 days), standard clinical and laboratory examination, peripheral arterial tonometry using the «EndoPAT 2000» apparatus, and psychological testing using validated questionnaires (hospital anxiety and depression scale and Beck depression scale) were performed. RESULTS: The integrated model for predicting the risk of acute heart failure (AHF) development (pulmonary edema and cardiogenic shock) identified admission LVEF as the leading prognostic parameter. With LVEF ≤40.5%, the probability of AHF in patients with TS in the acute period was 62.5%, and in patients with TS and QTc interval 487 ms, the risk reached 100%. The sensitivity and specificity of the developed model were 72.7% and 97.4%, respectively. The integrated model for predicting the development of cardiovascular complications (CVCs) revealed that the number of leukocytes in the peripheral blood was the leading risk factor for adverse events in patients with TS in the acute period. With a leukocyte count 11.1×109/L, the risk of CVCs in patients with TS increased to 89.9%, and if the erythrocyte count was 4.69×1012/L or ≤4.29×1012/L, it could reach 100%. The sensitivity and specificity of the resulting model were 92.6 and 97.0%, respectively. CONCLUSION: The models proposed in this study for predicting the likelihood of developing severe AHF and the overall risk of CVCs in the acute period of TS are personalized and easy to use, allowing for the selection of optimized treatment techniques

    Features of endothelial function and autonomic regulation of heart rhytm in patients with vasospastic angina

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    BACKGROUND: The clinical features of vasospastic angina are well known, but pathogenesis remains a subject of discussion. Changes in the autonomic regulation of coronary artery tone and endothelial function that contribute to the development of vasospasm are not well understood. The data on the subject from the published studies are contradictory.&#x0D; AIM: To evaluate features of endothelial function and autonomic regulation of heart rhythm in patients with vasospastic angina.&#x0D; MATERIALS AND METHODS: The study included 16 patients with proven vasospastic angina. All the patients have been evaluated for the heart rate variability at rest and vegetative tests (deep breathing, and active standing tests). Endothelial function has been assessed in terms of reactive hyperemia index by peripheral arterial tonometry using an Endo-PAT 2000 device.&#x0D; RESULTS: The baseline of the total heart rate variability was borderline with the normal parameters SDNN 50 (32.5; 50) ms in the patients with vasospastic angina. There were 14 patients who have demonstrated an imbalance of the autonomic nervous system at rest, mainly due to an increase of parasympathetic influences. The appropriate reaction of the autonomic nervous system, characterized by an increase of vagal influences, has been determined in 13 patients in the deep-breathing test. A paradoxical reaction, characterized by an increase of vagal influences on the heart rhythm, has been registered in 13 patients in the active standing tests. Endothelial dysfunction has been observed in half of the studied patients. Furthermore, a combination of both pathophysiological mechanisms, i.e., endothelial and autonomic dysfunctions have been observed in all the patients with a reduced reactive hyperemia index.&#x0D; CONCLUSIONS: According to the results of our study, the parasympathetic influences of the autonomic nervous system on the heart rhythm were predominant in the patients with vasospastic angina, which is not typical for coronary heart disease. All the patients had autonomic or endothelial dysfunction. A combination of both pathophysiological mechanisms has been observed in half of the examined patients.</jats:p

    Systemic transtiretin amyloidosis in the elderly patient with recurrent pleural effusions

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    Systemic amyloidosis is a group of diseases associated with extracellular deposition of fibrillar proteins, which leads to a loss of normal organ structure and function. Transthyretin amyloidosis occurs with the deposition of amyloid, consisting of transthyretin transport protein, and can be a genetic or degenerative disease of senility (acquired from the deposition of wild-type transthyretin).&#x0D; The article describes the clinical case of transthyretine amyloidosis in elderly patient, manifested by recurrent pleural effusions and biventricular heart failure demonstrating the complexity of timely diagnosis of wild-type transthyretin amyloidosis.</jats:p
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