Intramyocardial Arteries Research Articles

EFFECT OF HIGH INTENSITY TRAINING ON CARDIAC ALLOGRAFT VASCULOPATHY ASSESSED WITH OPTICAL COHORENCE TOMOGRAPHY

Cardiac allograft vasculopathy (CAV) is a distinct form of accelerated cardiovascular disease and a leading cause of long-term mortality after heart transplantation (HTx). It is characterized by concentric intima hyperplasia affecting both epicardial and intramyocardial arteries. In the HITTS

Coronary microvascular remodelling in low oxygen microenvironment: Role of cilnidipine, a dual L/N type calcium channel blocker

Background: People exposed to chronic sustained hypoxia (COPD) ultimately succumb to cardiovascular diseases. The heart is an obligate aerobic organ that requires a continuous supply of oxygen for its normal functions. Hence the structural and functional integrity of coronary microvasculature is very crucial for the normal functioning of the myocardium. Aims and Objectives: To assess the coronary microvascular remodelling in chronic sustained hypoxia exposure and its association with hypoxia signalling molecules. To study the role of cilnidipine, a unique calcium channel blocker (CCB) with dual L/N type calcium channel blocking actions with a documented cardioprotective role on chronic hypoxia-induced coronary microvascular remodelling. Methodology: 24 Wistar strain albino rats were randomly allocated into one of the four groups as follows - group 1, Control, (Normoxia, 21% O2); group 2, Chronic Hypoxia (CH) (10% O2, 90% N); group 3, Normoxia (21% O2) + Cilnidipine (Cil); group 4, Chronic Hypoxia (10% O2, 90% N) + Cilnidipine (CH+Cil). The intervention period was 21 days. Coronary microvascular remodelling was assessed by histopathological examination of the intramyocardial coronary artery. Normalised wall index (NWI) which is an indicator of arterial remodelling was calculated using histological images of coronary microvasculature using ImageJ software ( https://imagej.nih.gov/ij/ ). Hypoxia signalling molecules like vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (NOS3), nitric oxide (NO) were estimated in the serum and their correlation with NWI was determined. Results and Conclusion: Histopathological examination of intramyocardial coronary artery demonstrated moderate arteriosclerosis and congestion on CH exposure. NWI was significantly increased indicating an overall increase in wall thickness. NWI and VEGF and eNOS were positively correlated. Cilnidipine treatment ameliorated the chronic hypoxia-induced coronary microvascular remodelling. Hence chronic hypoxia-induced coronary microvascular remodelling may be an early subclinical culprit in the pathogenesis of CVDs in patients exposed to hypoxia. The present study also reiterates the cardioprotective role of cilnidipine while opening new avenues for its role in coronary microvasculature in chronic hypoxia exposure.

Microvascular Contractile Dysfunction Associates with a Synthetic Phenotype of Human Intramyocardial Artery Smooth Muscle Cells

Microvascular Contractile Dysfunction Associates with a Synthetic Phenotype of Human Intramyocardial Artery Smooth Muscle Cells

Microvascular Contractile Dysfunction Associates with a Synthetic Phenotype of Human Intramyocardial Artery Smooth Muscle Cells

Microvascular Contractile Dysfunction Associates with a Synthetic Phenotype of Human Intramyocardial Artery Smooth Muscle Cells

Pathological changes of myocardium in the model of chronic renal insufficiency at application of low-protein diet

Myocardial damage in patients with chronic renal failure histologically manifests as hypertrophy of cardiomyocytes, intramyocardial artery walls, development of diffuse sclerosis and a change in the number of capillaries. One of the components in the complex treatment of this category of patients is a low-protein diet, however, to date there is no data on the effect of a low-protein diet on structural changes in the myocardium. The aim of the work was to assess the effect of low protein diet on myocardial structural changes in the experimental model of chronic renal failure. To reproduce the experiment of chronic renal failure, a standardized 5/6 nephrectomy model was used in wistar rats. To determine the effect of a low-protein diet on structural changes in the myocardium, two types of diet were used - a standard one and a low-protein diet (Ketosteril). The animals were sacrificed 4 months after nephrectomy. For a comparative assessment of the effect of low-protein diet on structural changes in the myocardium, histological methods of investigation and morphometry were used. The use of low-protein diet was accompanied by a less pronounced violation of biochemical blood parameters (creatinine, urea, calcium, phosphorus), as well as maintaining normal blood pressure, myocardial mass and left ventricular wall thickness. Histologically, this was manifested by a decrease in the severity of dystrophic changes in cardiomyocytes, the degree of their hypertrophy, a decrease in the area of nuclei, and a decrease in the nuclear-cytoplasmic ratio. Indices of perivascular and diffuse sclerosis were lower compared with the control group. Also, when using low-protein diet in animals with a chronic renal failure model, a decrease in the total cross-sectional area of capillaries was noted with an increase in their number in comparison with animals of the control group. Thus, the use of a low-protein diet in an experimental model of chronic renal failure has a cardioprotective effect by reducing the severity of uremia and stabilizing biochemical parameters.

Impact of a Multichannel Blocker in Attenuating Intramyocardial Artery Remodeling in Hypertensive Rats through Increased Nitric Oxide Bioavailability.

Dronedarone is recommended for the treatment of atrial fibrillation. However, we do not know its effect on vascular remodeling. This study was designed to assess whether dronedarone has the potential to improve the intramyocardial artery remodeling induced by chronic hypertension. Ten-month-old male spontaneously hypertensive rats (SHR) were randomly assigned to receive dronedarone (100 mg/kg) or vehicle. Age-matched male Wistar-Kyoto rats served as controls. After 14 days of treatment, we studied the structure (geometry and fibrosis) of the intramyocardial artery using histological analysis. Nitric oxide (NO) in plasma was analyzed. In the untreated SHR, we observed a significant increase in external diameter, lumen diameter, wall width, cross-sectional area, and collagen volume density, as was expected in the experimental model. Dronedarone induced a significant decrease in wall width, cross-sectional area, and collagen volume density in SHR-D in comparison with untreated SHR. The values obtained in SHR-D were similar in the WKY control group. We found significantly higher NO levels in plasma in SHR-D than in untreated SHR. Dronedarone improves the intramyocardial artery remodeling induced by chronic hypertension in SHR through increased nitric oxide bioavailability.

Does gender influence cardiovascular remodeling in C57BL/6J mice fed a high-fat, high-sucrose and high-salt diet?

Animal models are widely used to study the physiopathology of human diseases. However, the influence of gender on modern society diet style-induced cardiovascular disease has not thus far been explored in these models. Thus, this study investigated cardiovascular remodelling in C57BL/6J mice fed a diet rich in saturated fat, sucrose and salt, evaluating gender effect on this process. Male and female C57BL/6J mice were fed AIN93M diet or a modified AIN93M rich in fat, sucrose and salt (HFSS) for 12weeks. Body mass, water and food intake and cardiovascular remodelling were assessed. The HFSS diet did not lead to body mass gain or glucose metabolism disturbance as assessed by serum glucose, insulin and oral glucose tolerance test. However, female mice on a HFSS diet had increased visceral and subcutaneous adiposity. Only male mice displayed heart hypertrophy. The left ventricle was not hypertrophied in either male or female mice, but its lumen was dilated. Intramyocardial arteries and the thoracic aorta showed media thickening in male mice, but in the female it was only observed in the thoracic aorta. Finally, intramyocardial artery dilation was present in both genders, but not in the aorta. Therefore changes in LV dimensions and arterial remodelling were influenced by both gender and the HFSS diet. In conclusion, male and female C57BL/6J mice suffered cardiovascular remodelling after 12weeks of HFSS feeding, although they did not develop obesity or diabetes. Sexual dimorphism occurred in response to diet for body adiposity, heart hypertrophy and intramyocardial artery remodelling.

Carthamus Tinctorius L. extract attenuates cardiac remodeling in L-NAME-induced hypertensive rats by inhibiting the NADPH oxidase-mediated TGF-β1 and MMP-9 pathway

Carthamus tinctorius L. (CT) has been widely used in Asian countries as a beverage and a folk medicine. The current study investigates the effect of CT extract on cardiac remodeling and possible mechanisms involved in Nw-nitro-l-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. Male Sprague-Dawley rats were administrated with L-NAME (40mg/kg/day) for five weeks to induce hypertension. Hypertensive rats were treated with CT extract (300mg/kg/day) or captopril (5mg/kg/day) or vehicle for a further two weeks. Treatment of hypertensive rats with CT extract or captopril significantly decreased systolic blood pressure, left ventricular (LV) hypertrophy and fibrosis, small intramyocardial coronary artery remodeling, and cardiac weight index. CT extract or captopril increased plasma nitric oxide metabolite (NOx) levels and reduced plasma transforming growth factor β1 (TGF-β1) level, together with downregulation of cardiac TGF-β1 and matrix metalloproteinases-9 (MMP-9) expression. In addition, decreased plasma malondialdehyde (MDA) levels, consistent with downregulation of NADPH oxidase subunit gp91phox expression in heart tissue, was also observed after CT extract or captopril treatment. These findings suggest that CT extract alleviates cardiac remodeling in L-NAME-induced hypertensive rats, which is possibly related to inhibition of the NADPH oxidase-mediated TGF-β1-MMP-9 pathway.

3273Expression of lectin-like oxidized low-density lipoprotein receptor-1 in human epicardial and intramyocardial coronary arteries of male patients undergoing coronary artery bypass grafting

3273Expression of lectin-like oxidized low-density lipoprotein receptor-1 in human epicardial and intramyocardial coronary arteries of male patients undergoing coronary artery bypass grafting

INTRAMYOCARDIAL CORONARY ARTERIES IN CHILDREN: NOT ALL ARE BENIGN BUT MOST ALLOW RETURN TO EXERCISE

Intramyocardial (IM) coronary arteries are characterized by a segment of a coronary artery (CA) that travels into the myocardium instead of the normal epicardial course. It may occur in isolation or in association with anomalous aortic origin of a CA (AAOCA). They are uncommon lesions in children

Expression of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 in Human Epicardial and Intramyocardial Coronary Arteries of Male Patients Undergoing Coronary Artery Bypass Grafting

Objectives: Atherosclerosis is almost absent in intramyocardial coronary arteries, while epicardial coronary arteries may show extensive occlusive disease. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) expression has been implicated in atherogenesis. We aimed to investigate differences in arterial wall LOX-1 expression between human epicardial and intramyocardial coronary arteries. Methods: Epicardial and intramyocardial total artery wall specimens were obtained from 13 male patients (aged 61.9 ± 10.3 years) undergoing coronary artery bypass graft surgery due to 3-vessel coronary artery disease. LOX-1 expression was examined by reverse transcription-polymerase chain reaction. Results: LOX-1 expression was significantly higher in the arterial wall of epicardial coronary arteries compared to intramyocardial coronary arteries. The LOX-1/GAPDH ratio was 0.48 ± 0.07 vs. 0.35 ± 0.03 (p < 0.001). Conclusions: Our findings may partially explain the atheroprotective effect of the intramyocardial course since arterial wall LOX-1 expression was lower in intramyocardial arteries and higher in epicardial coronary arteries.

Monoamine oxidase A inhibition protects the myocardium after experimental acute volume overload.

Objective:The molecular pathway leading to myocardial cellular destruction after acute volume overload (AVO) may include monoamine oxidases. The aim of the present study was to investigate whether moclobemide (Mo), a monoamine oxidase inhibitor, protects the myocardium after AVO.Methods:Sixty syngeneic Fischer rats underwent surgical abdominal aortocaval fistula to induce AVO. Eighteen rats were treated with Mo 10 mg/kg/day and were compared with 42 untreated rats with AVO without treatment. Myocardial recovery was analyzed using quantitative reverse transcription polymerase chain reaction for hypoxia-inducible factor 1-alpha, inducible nitric oxide synthase, interleukin 6, E-selectin, atrial natriuretic peptide (ANP), brain natriuretic peptide, vascular endothelial growth factor-alpha, matrix metalloproteinase 9, chitinase 3-like protein (YKL-40), and transforming growth factor-beta.Results:After 3 days, the relative number of ischemic intramyocardial arteries in the left ventricle was lower in AVO treated with Mo than in without [0.04 (0.02–0.07) vs. 0.09 (0.07–0.14), point score unit]. After 1 day, ANP was lower in AVO treated with Mo than in without [0.95 (0.37–1.84) vs. 2.40 (1.33–3.09), fold changes from the baseline (FC), p=0.044], whereas after 1 and 3 days, YKL-40 was higher in AVO treated with Mo than in without [22.66 (14.05–28.83) vs. 10.06 (6.23–15.02), FC, p=0.006 and 6.03 (4.72–7.18) vs. 3.70 (2.62–5.35), FC, p=0.025].Conclusion:Mo decreases intramyocardial arterial ischemia of the left ventricle after AVO while increases YKL-40, reflecting cellular protection during early cardiac remodeling. In the future, adding Mo may be a simple means for myocardial protection after AVO. (Anatol J Cardiol 2019; 21: 39-45)

Surgical Acute Volume-Overload Impacts Early on Myocardium - An Experimental Study.

Acute volume-overload (AVO) predisposes to cardiac failure. Global cardiac injury may ensue after acute right-sided distension of the heart due to AVO. We experimentally investigated whether surgical AVO impacts early on the myocardium and some markers of injury. Thirty-four syngeneic Fisher rats underwent surgical abdominal aortocaval fistula to induce AVO. The hearts were procured for regional and quantitative histology after one and three days. Gene expressions for atrial natriuretic peptide (ANP), matrix metalloprotease 9 (MMP9), transforming growth factor β (TGFβ) and YKL40 were investigated for myocardial injury. The relative number of ischemic intramyocardial arteries were abundant in the septum of the hearts with AVO compared with controls at day 1 and 3 [0.16 ± 0.02 vs. 0.02 ± 0.01, point score unit (PSU), p = 0.002 and 0.14 ± 0.02 vs. 0.02 ± 0.01, PSU, p = 0.009, respectively] followed by similar changes in the left ventricle at day 3 (0.11 ± 0.02 vs. 0.04 ± 0.01, PSU, p = 0.007). Indicating early myocardial injury, ANP (p = 0.019) was increased in AVO hearts as compared with controls at day 1, as expected. More interestingly, MMP9 (p = 0.003 and p = 0.006), TGFβ (p = 0.002 and p = 0.004) and YKL40 (p = 0.001 and p = 0.003) expressions were significantly increased at day 1 and 3, along with macrophage infiltration into the myocardium supporting the role of factors produced by alternatively activated macrophages in the pathogenesis of AVO-induced pathophysiology in the heart. Surgical AVO induces an early ischemic myocardial response observed in the intramyocardial arteries. Early expression of key parameters of cardiac remodeling suggest for the onset of early cardiac failure after AVO.

Speculative Considerations about Some Cardiology Enigmas.

Background:Enigmas often lead to hypotheses and speculations. For this reason, especially for the sake of the reader’s motivation, we opted for the plain discussion of some cardiology enigmas.Objective:The present text was aimed to discuss speculatively some cardiology enigmas.Method:Text was freely designed in the context of coronary artery and heart valve diseases.Results:The results were presented as the combination enigma/hypothesis. 1) The absence of arteriosclerosis in intramyocardial coronary arteries/ endothelium-myocardial interaction (crosstalk); 2) The unique and always confirmed superior evolution of the internal thoracic artery as coronary graft/ higher NO basal release 3) The prophylactic left internal thoracic artery graft in mildly-stenosed coronary lesions/need of more accurate functional imaging techniques; 4) The high incidence of perioperative atrial fibrillation in patients with coronary artery disease/atrial ischemia associated to left circumflex coronary lesions; 5) The handling of disease-free saphenous vein grafts at the time of re-operation/biological serendipity with graft vein segments; 6) The possible aortic stenosis protection against coronary artery disease/ endothelium myocardium interaction (crosstalk) improving NO release.Conclusion:The discussed topics associated with their respective speculative hypothesis remain as enigmas, but would become motivations for investigations

Adverse remodeling of the obtuse marginal artery in compensatory hypertrophied myocardium from spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) serve as a model of genetic hypertension. Adverse remodeling of a coronary artery has been reported in SHR. This model is used to study new therapies in regression vascular remodeling. However, no data are available that show remodeling of the intramyocardial branch of the obtuse marginal artery in 10-month-old SHR. This study was designed to assess remodeling (changes in vascular structure and fibrosis) of this coronary artery. The study was performed on 10-month-old male SHR (n=7) and normotensive control Wistar Kyoto rats (WKY) (n=7). Using histology, we show that the external diameter, lumen diameter, wall width, and cross-sectional area of the intramyocardial artery were significantly greater in SHR than in WKY. The wall-to-lumen ratio was similar in SHR and WKY. The collagen volume density of the intramyocardial artery in SHR was significantly greater than in WKY. Our results show hypertrophic outward remodeling in the intramyocardial branch of the obtuse marginal artery of the left ventricle in SHR. This artery can serve as a new vascular bed from adult SHR to study novel therapies in regression coronary artery remodeling.

CXCL12 And Vascular Maturation Of The Coronary System During Heart Development

Elucidating the mechanisms involved in the patterning of coronary blood vessels in the embryo will help to improve therapies for coronary perfusion in the injured heart. In the past few years, there have been significant efforts and advances in the understanding of coronary vessel development. The major endothelial cell sources that provide coronary endothelial progenitors to the heart are the sinus venosus (the vein that delivers the venous return) and the endocardium, although the respective contribution from each source is debated. Angiogenic sprouts from the sinus venosus reach the ventricles starting at E11.5 in the mouse and form a vascular plexus in the subepicardial space. This primitive plexus undergoes a complex and incompletely understood process of vascular maturation that involves pruning, branching and reorganization into a hierarchical network of superficial veins and intramyocardial arteries. The main branches of the coronary arteries ultimately connect to the aorta through the coronary ostia by E13.5 – E14.0.CXCL12 (also known as stromal derived factor 1, SDF1) is a chemokine that acts through the G protein‐coupled receptor CXCR4. Global deficiency of Cxcl12 or Cxcr4 as well as endothelial deletion of Cxcr4 result in vascular defects in the mouse kidney and gut, but these defects do not explain the associated late gestation lethality. We hypothesized that coronary vascular defects might underlie the embryonic lethality of CXCL12 deficiency.Cxcl12 and Tie2Cre/Cxcr4 mutants form an initial coronary vascular plexus, which then fails to remodel into a hierarchical network of mature vessels, resulting in the absence of the major intramyocardial coronary arteries, hemorrhage and reduced ventricular wall perfusion. The coronary veins were mostly unaffected, and the basis of the selectivity of CXCL12 on the arterial side of the vasculature is still unclear.In vitro, CXCL12 does not induce sprouting of endothelial cells from beads embedded in a fibrin gel matrix, but instead promotes maturation of vascular sprouts preformed in response to VEGF, by increasing tube elongation, vessel branching, anastomosis and intussusception, all features of mature blood vessel networks. These features were abolished in the presence of AMD3100, a CXCR4 inhibitor. Thus, CXCL12 does not initiate vasculogenesis but rather promotes further remodeling of a plexus that is initially induced by VEGF.We conclude that failed maturation of the coronary system explains the late‐gestation lethality of Cxcl12 mutants, and highlight the role of CXCL12 as an organ‐specific arterial maturation factor of particular relevance in the coronary vasculature. Our current studies are aimed at defining the role of CXCL12 in reprogramming of venous endothelial cells from the sinus venosus into coronary arterial endothelium.Support or Funding InformationThis work was supported by NIH grant HL070123 to H.M.S. and grant 14BGIA20500059 to S.R.K. from the American Heart Association. S.C. was supported by a Postdoctoral Fellowship from the American Heart Association. H.S. was supported by a Postdoctoral Fellowship from the California Institute for Regenerative Medicine.

Myocardial effects of fetal endoscopic tracheal occlusion in lambs with CDH.

Fetal endoscopic tracheal occlusion in congenital diaphragmatic hernia (CDH) may reduce pulmonary hypertension and ameliorate postnatal cardiac output. The effects of sustained early (ETO) and late (LTO) tracheal occlusion on left ventricular (LV) cells in the lamb model have not been described. CDH was created in lambs at 70 days' gestation (term = 145 days). ETO (85 days) or LTO (105 days) was sustained till term. After cesarean section (140 days) fetuses were euthanized and hearts harvested. LV myocardial cells were studied by histological and immunofluorescence (TGF-beta 1, endothelin-1) assays in CDH, ETO, LTO, and the control group (two subjects per group). Small intramyocardial arteries were evaluated by traditional histology. LV myocardial histology in CDH and LTO was similar. ETO-induced LV myocardial cell enlargement and increased endothelin-1 and TGF-beta 1 staining; a weaker immunofluorescence signal was observed in LTO compared with ETO. Myocardial vascular wall thickness was greater in CDH than in controls. ETO was associated with a vascular wall thickness within the range of controls. With only two fetuses in each group, only an explorative evaluation was possible. The time point at which TO is performed seems to have an effect on cardiac morphology. Functional studies as well as confirmation in clinical samples are mandatory.

Off-pump coronary artery bypass surgery: Intra-aortic balloon pump aides multivessel revascularization in high-risk patients

Objective: Off-pump coronary artery bypass (OPCAB) has been demonstrated to be a safe technique with similar outcomes to on-pump coronary artery bypass (ONCAB) in low-risk patients, while its role and benefits in high-risk patients are the subject of ongoing clinical trials. This review compares our high-risk patients aided by intra-aortic balloon pump (IABP) with low-risk patients undergoing OPCAB to identify any differences in outcomes. Materials and Methods: One hundred and twenty-four patients who underwent OPCAB surgery between January 2004 and December 2013 were retrospectively reviewed. 61.3% were males, 57.3% were African Americans, mean age was 62.7 ± 13.3, and range was 30-90 years. Patients were divided into Group 1, 26 (21.0%) patients with IABP and Group 2, 98 (79.0%) patients without IABP. Group 1 patients had higher risk profile with mean ejection fraction (EF) 26.0 ± 10.8 and EF ≤20 present in 46.1% compared to 45.2 ± 11.9 and 5.1%, respectively, in Group 2 (P < 0.001). Results: 92.35% of Group 1 and 82.7% of Group 2 patients had multivessel disease with a mean number of bypass grafts 2.9 ± 0.97 versus 2.75 ± 0.8, respectively (P < 0.364). Left internal mammary artery (LIMA) to left anterior descending (LAD) was performed in all Group 1 and 97.9% of Group 2 patients, with saphenous vein graft (SVG) to the left circumflex and right coronary arteries in 73.1% versus 62.2% and 57.7% versus 52.0% of Groups 1 and 2, respectively. Complete revascularization occurred in 88.5% and 90.8% of Groups 1 and 2, respectively (P < 0.990). 4.0% were converted to ONCAB for either hemodynamic instability or intramyocardial coronary artery. Major morbidities were re-exploration for bleeding 3.8% versus 1.0%, stroke 3.8% versus 2.0%, acute kidney injury 11.5% versus 0%, and prolonged intubation 15.4% versus 2.0% in Groups 1 and 2, respectively. Euroscore II predicted (P) versus observed (O) mortality was 4.56% versus 4.03%, for Group 1, 7.82% versus 7.69% and Group 2, 3.64% versus 3.06%, and O/P ratios 0.88, 0.98 and 0.84 respectively. Two (2.0%) females in Group 2 with single LIMA to LAD underwent repeat revascularization with SVG to the LAD within 90 days. Conclusion: IABP helps stabilize hemodynamics during OPCAB in high-risk patients with moderate to severe left ventricular dysfunction. Mean number of bypass grafts and predicted versus observed mortality were similar between the low- and high-risk groups.

MYOCARDIAL INFARCTION AS TYPICAL PRESENTATION OF NONCOMPACTION CARDIOMYOPATHY

The main clinical presentation of noncompaction myocardium (NCM) as nosologic unit are thromboembolic syndrome, heart failure, mostly ventricular arrhythmias and ischemia itself, related to insufficient myocardium blood supply under the noncompacted layer. Also, there are only sporadic cases of myocardial infarction described (MI), including “idiopathic”, in NCM. Aim. To check the prevalence of acute MI in patients with NCM, the specialties of clinical picture, diagnostics, and its probable specific mechanisms, influence on prognosis and its ways of prevention. Material and methods. Totally, 10 patients included, 7 males and 3 females, mean age — 46,3±15,8 y. o., (30 to 76 y. o.) among 85 patients with verified NCM diagnosis, set in accordance with harmonized visual criteria, and developed MI on this background. In 4 cases the NCM is confirmed with three visualizing criteria (EchoCG, MSCT, MRI of the heart), in 4 other — with the two. Mean follow-up was 10,5 [1,75; 32,25] months — from 1 month to 1 year. All patients underwent ECG, ambulatory ECG recording by Holter, EchoCG, assessment of antibodies against various heart antigens, PCR for DNA of parvovirus and B19, as well as herpes group, in blood; 7 coronary arteriographies, 7 MSCT of the heart, measurement of Troponin (n=7), morphological investigation of the heart with PCR-diagnostic of viral infection (n=6), MRI (n=5) and myocardium scintigraphy with 99mТс (n=6). Results . In 4 among 10 patients the development of MI was the first presentation of NCM. Prevalence of coronary atherosclerosis in those with MI and NCM was 20%, however in most cases development of MI was not related with coronary atherosclerosis. Intracardiac thrombosis was verified in 60% of patients with MI, embolism to other organs in 30%. The following mechanisms of MI established: 1) thromboembolism to coronary arteries if thrombi are present in the left chambers of the heart (atrium a. w.a. ventricle), verified in 1 patient at autopsy, and is suspected in other five; 2) concomitance of myocarditis, incl. viral, with microvasculitis development and thrombosis of intramyocardial arteries and focal necrosis in ischemized myocardium (n=6); 3) thrombosis of coronary arteries with presence of hemodynamically significant atherosclerosis (probably 1 patient); 4) sudden worsening of blood supply under noncompacted layer under the circumstances of low cardiac output by secondary origins. Conclusion. MI is typical and unrare complication of NCM: its prevalence reached 11,8% in separate registry of 85 patients with NCM syndrome. Four probable mechanisms of MI (necrosis) in NCM (embolism, thrombosis, myocarditis, microcirculation disorder) might be comorbid. The development of MI leads to serious worsening of the baseline systolic dysfunction and ventricular rhythm disorders: mortality among MI patients with NCM is 20% with the mean time of follow-up 10,5 months. As a preventive matter against MI in NCM should be concerned the anticoagulants at least for atrial fibrillation and in systolic dysfunction, on-time diagnostics and myocarditis management.

MYOCARDIAL INFARCTION AS TYPICAL PRESENTATION OF NONCOMPACTION CARDIOMYOPATHY

The main clinical presentation of noncompaction myocardium (NCM) as nosologic unit are thromboembolic syndrome, heart failure, mostly ventricular arrhythmias and ischemia itself, related to insufficient myocardium blood supply under the noncompacted layer. Also, there are only sporadic cases of myocardial infarction described (MI), including “idiopathic”, in NCM. Aim. To check the prevalence of acute MI in patients with NCM, the specialties of clinical picture, diagnostics, and its probable specific mechanisms, influence on prognosis and its ways of prevention. Material and methods. Totally, 10 patients included, 7 males and 3 females, mean age — 46,3±15,8 y. o., (30 to 76 y. o.) among 85 patients with verified NCM diagnosis, set in accordance with harmonized visual criteria, and developed MI on this background. In 4 cases the NCM is confirmed with three visualizing criteria (EchoCG, MSCT, MRI of the heart), in 4 other — with the two. Mean follow-up was 10,5 [1,75; 32,25] months — from 1 month to 1 year. All patients underwent ECG, ambulatory ECG recording by Holter, EchoCG, assessment of antibodies against various heart antigens, PCR for DNA of parvovirus and B19, as well as herpes group, in blood; 7 coronary arteriographies, 7 MSCT of the heart, measurement of Troponin (n=7), morphological investigation of the heart with PCR-diagnostic of viral infection (n=6), MRI (n=5) and myocardium scintigraphy with 99mТс (n=6). Results . In 4 among 10 patients the development of MI was the first presentation of NCM. Prevalence of coronary atherosclerosis in those with MI and NCM was 20%, however in most cases development of MI was not related with coronary atherosclerosis. Intracardiac thrombosis was verified in 60% of patients with MI, embolism to other organs in 30%. The following mechanisms of MI established: 1) thromboembolism to coronary arteries if thrombi are present in the left chambers of the heart (atrium a. w.a. ventricle), verified in 1 patient at autopsy, and is suspected in other five; 2) concomitance of myocarditis, incl. viral, with microvasculitis development and thrombosis of intramyocardial arteries and focal necrosis in ischemized myocardium (n=6); 3) thrombosis of coronary arteries with presence of hemodynamically significant atherosclerosis (probably 1 patient); 4) sudden worsening of blood supply under noncompacted layer under the circumstances of low cardiac output by secondary origins. Conclusion. MI is typical and unrare complication of NCM: its prevalence reached 11,8% in separate registry of 85 patients with NCM syndrome. Four probable mechanisms of MI (necrosis) in NCM (embolism, thrombosis, myocarditis, microcirculation disorder) might be comorbid. The development of MI leads to serious worsening of the baseline systolic dysfunction and ventricular rhythm disorders: mortality among MI patients with NCM is 20% with the mean time of follow-up 10,5 months. As a preventive matter against MI in NCM should be concerned the anticoagulants at least for atrial fibrillation and in systolic dysfunction, on-time diagnostics and myocarditis management.