Focal Myocardial Infarction Research Articles

Layer-specific proteomic profiling of human normal heart

BackgroundThe organized functioning of the anisotropic myocardial layers—including the inner longitudinal, middle circular, and outer longitudinal layers—is essential for stable systemic circulation. However, the proteomic profile of each myocardial layer has not been studied yet. Here, we aimed to elucidate the layer-specific proteomic profile of human cardiac tissue using microscopic sampling. MethodsNormal hearts were obtained from five autopsy cases, and cardiomyocytes were microdissected separately from the three myocardial layers of the left ventricle. Histological analysis and shotgun proteomic profiling were performed, followed by immunohistochemical analysis. ResultsHistologically, no significant changes were observed among the three layers regarding cardiomyocyte diameter and myocardial fibrosis. Totally 1220 proteins—comprising 9404 peptides—were identified from 15 samples, of which the expression levels of 92 proteins were significantly altered among the layers. Gene ontology enrichment analysis revealed that the proteins specifically elevated in the inner and outer layers mostly belonged to the actin filament-binding protein group. In particular, MYH1 was highly expressed in cardiomyocytes in the outer layer, and CTNNA3 was highly expressed at the intercalated disc in the inner layer. ConclusionsThis is the first report on layer-specific proteomic profiling of human normal hearts. Anisotropic profiles of actin filament-binding proteins in myocardial layers may contribute to the anisotropic contractile and conductive abilities of the heart. Knowledge of the layer-specific proteome profiles of a human heart in the normal state can aid in further research on cardiac pathology, such as the prognosis and treatment of focal myocardial infarction.

Small focal myocardial infarction and chronic hepatitis at the expanded plenary meeting of the All-Russian Society of Physicians

In the program report "On the intermediate forms between angina pectoris and myocardial infarction" prof. AL Myasnikov emphasized that these forms are approved by life itself.

Regenerative Potential of a Suspension and Spheroids of Multipotent Mesenchymal Stromal Cells from Human Umbilical Cord on the Model of Myocardial Infarction in Rats

Regenerative potential of multipotent mesenchymal stromal cells from the human umbilical cord (MMSC-UC) in the suspension and spheroid form was revealed during the progression of experimental small focal myocardial infarction in rats. In isoproterenol-induced myocardial infarction, foci of necrosis and inflammatory infiltrate and at later terms fibrosis foci were found mainly in the left ventricle of rat heart. In rats receiving MMSC-UC, destructive changes in the myocardium, fibrous scars, and inflammatory process were less pronounced. MMSC-UC also contributed to normalization of the morphofunctional parameters of the heart. Spheroids exhibited higher efficiency in comparison with cell suspension.

Post-procedural myocardial infarction following surgical aortic valve replacement and transcatheter aortic valve implantation

Myocardial injury assessed using cardiac biomarker release is ubiquitous following surgical aortic valve replacement (SAVR) and transcatheter aortic valve implantation (TAVI), preventing accurate discrimination between focal myocardial infarction (MI) and global injury. Cardiovascular magnetic resonance (CMR) late gadolinium enhancement (LGE) imaging was used to compare rates of new MI following SAVR and TAVI. Identical CMR scans were obtained at baseline and six months post procedure in ninety-six patients undergoing SAVR (n=39) and TAVI (n=57). The rate of new MI was greater following SAVR than TAVI (SAVR, n=10 [26%] vs. TAVI, n=3 [5%], p=0.004). Infarct mass was similar between groups (SAVR 1.1±0.6 vs. TAVI 2.0±1.4 g, p=0.395). New MI did not impact on change in LV ejection fraction (SAVR:LGE[+]2.2±4.7 vs. LGE[-]0.9±8.0%, p=0.437, TAVI:LGE[+]-0.9±6.0 vs. LGE[-]2.0±7.8%, p=0.420). Thirty-four patients (60%) in the TAVI group had non-revascularised coronary artery disease (CAD) at the time of TAVI, of whom three (9%) had new MI. MI is an infrequent complication of TAVI but is more common following SAVR. Infarct size is small following both procedures. The low new infarct rate in TAVI, especially in the context of high rates of non-revascularised CAD, strengthens data from previous studies suggesting that coronary revascularisation pre-TAVI may be unnecessary.

Post-procedural myocardial infarction following surgical and trans-catheter aortic valve replacement - mechanistic insights from cardiovascular magnetic resonance imaging

Background Cardiac biomarker release is ubiquitous following surgical and transcatheter aortic valve replacement (SAVR and TAVR), preventing accurate discrimination between release due to focal myocardial infarction (MI) and global myocardial injury. Cardiovascular magnetic resonance (CMR) late gadolinium enhancement imaging (LGE) is the most sensitive imaging method to detect post-procedural new MI. Our study aimed to compare rates of new MI using CMR LGE before and 6m after TAVR and SAVR.

Non-invasive technology that improves cardiac function after experimental myocardial infarction: Whole Body Periodic Acceleration (pGz).

Myocardial infarction (MI) may produce significant inflammatory changes and adverse ventricular remodeling leading to heart failure and premature death. Pharmacologic, stem cell transplantation, and exercise have not halted the inexorable rise in the prevalence and great economic costs of heart failure despite extensive investigations of such treatments. New therapeutic modalities are needed. Whole Body Periodic Acceleration (pGz) is a non-invasive technology that increases pulsatile shear stress to the endothelium thereby producing several beneficial cardiovascular effects as demonstrated in animal models, normal humans and patients with heart disease. pGz upregulates endothelial derived nitric oxide synthase (eNOS) and its phosphorylation (p-eNOS) to improve myocardial function in models of myocardial stunning and preconditioning. Here we test whether pGz applied chronically after focal myocardial infarction in rats improves functional outcomes from MI. Focal MI was produced by left coronary artery ligation. One day after ligation animals were randomized to receive daily treatments of pGz for four weeks (MI-pGz) or serve as controls (MI-CONT), with an additional group as non-infarction controls (Sham). Echocardiograms and invasive pressure volume loop analysis were carried out. Infarct transmurality, myocardial fibrosis, and markers of inflammatory and anti-inflammatory cytokines were determined along with protein analysis of eNOS, p-eNOS and inducible nitric oxide synthase (iNOS).At four weeks, survival was 80% in MI-pGz vs 50% in MI-CONT (p< 0.01). Ejection fraction and fractional shortening and invasive pressure volume relation indices of afterload and contractility were significantly better in MI-pGz. The latter where associated with decreased infarct transmurality and decreased fibrosis along with increased eNOS, p-eNOS. Additionally, MI-pGz had significantly lower levels of iNOS, inflammatory cytokines (IL-6, TNF-α), and higher level of anti-inflammatory cytokine (IL-10). pGz improved survival and contractile performance, associated with improved myocardial remodeling. pGz may serve as a simple, safe, non-invasive therapeutic modality to improve myocardial function after MI.

Left Main Coronary Artery Dissection in Pediatric Sport-Related Chest Trauma

BackgroundTraumatic coronary artery dissection (CAD) after blunt chest trauma (BCT) is extremely rare, particularly in children. Among coronary dissections, left main coronary artery (LMCA) dissection is the least common, with only two pediatric cases reported previously. Manifestations of coronary dissections can range from ST segment changes to sudden death. However, these manifestations are not specific and can be present with other cardiac injuries. To our knowledge we present the first pediatric case of traumatic LMCA dissection after sport-related BCT that was treated successfully with coronary stenting. Case ReportA 14-year-old child sustained BCT during a baseball game. Early in the clinical course, he had episodes of ventricular dysrhythmias, diffuse ST changes, rising troponin I, and hemodynamic instability. Emergent cardiac catheterization revealed an LMCA dissection with extension into the proximal left anterior descending artery (LADA). A bare metal stent was placed from the LMCA to the LADA, which improved blood flow through the area of dissection. He has had almost full recovery of myocardial function and has been managed as an outpatient with oral heart failure and antiplatelet medications. Why Should an Emergency Physician Be Aware of This?Our case highlights that CAD, although rare, can occur after pediatric BCT. Pediatric emergency responders must have a heightened awareness that evidence of ongoing myocardial ischemia, such as evolving and focal myocardial infarction on electrocardiogram, persistent elevation or rising troponin I, and worsening cardiogenic shock, can represent a coronary event and warrant further evaluation. Cardiac catheterization can be both a diagnostic and therapeutic modality in such cases. Early recognition and management is vital for myocardial recovery.

Focal myocardial infarction induces global remodeling of cardiac sympathetic innervation: neural remodeling in a spatial context

Myocardial infarction (MI) induces neural and electrical remodeling at scar border zones. The impact of focal MI on global functional neural remodeling is not well understood. Sympathetic stimulation was performed in swine with anteroapical infarcts (MI; n = 9) and control swine (n = 9). A 56-electrode sock was placed over both ventricles to record electrograms at baseline and during left, right, and bilateral stellate ganglion stimulation. Activation recovery intervals (ARIs) were measured from electrograms. Global and regional ARI shortening, dispersion of repolarization, and activation propagation were assessed before and during sympathetic stimulation. At baseline, mean ARI was shorter in MI hearts than control hearts (365 ± 8 vs. 436 ± 9 ms, P < 0.0001), dispersion of repolarization was greater in MI versus control hearts (734 ± 123 vs. 362 ± 32 ms(2), P = 0.02), and the infarcted region in MI hearts showed longer ARIs than noninfarcted regions (406 ± 14 vs. 365 ± 8 ms, P = 0.027). In control animals, percent ARI shortening was greater on anterior than posterior walls during right stellate ganglion stimulation (P = 0.0001), whereas left stellate ganglion stimulation showed the reverse (P = 0.0003). In infarcted animals, this pattern was completely lost. In 50% of the animals studied, sympathetic stimulation, compared with baseline, significantly altered the direction of activation propagation emanating from the intramyocardial scar during pacing. In conclusion, focal distal anterior MI alters regional and global pattern of sympathetic innervation, resulting in shorter ARIs in infarcted hearts, greater repolarization dispersion, and altered activation propagation. These conditions may underlie the mechanisms by which arrhythmias are initiated when sympathetic tone is enhanced.

Nonalcoholic percutaneous transluminal septal ablation for hypertrophic cardiomyopathy with obstruction

The procedure presented describes an alternative way to avoid this rare but serious complication. By positioning a covered stent in the left anterior descending artery at the origin of the septal perforator branch, mechanical occlusion of the perforator branch is achieved. This results in focal myocardial infarction as evidenced by the relatively modest elevation in creatine kinase compared with alcoholic percutaneous transluminal septal myocardial ablation and thinning of the ventricular septum. Although in-stent restenosis as well as thrombosis should be considered, these complications are better treatable compared with alcohol leakage in the left anterior descending artery. Therefore, this new technique could be a valuable alternative in treating obstructive HC.

Modulation of Nucleotide Triphosphate Diphosphohydrolase-1 (NTPDase-1)/cd39 in Xenograft Rejection

There is increasing evidence showing that extracellular nucleosides [corrected] may be important mediators of vascular inflammation. Nucleoside [corrected] triphosphate diphosphohydrolase-1 (NTPDase-1, identical to CD39), the major vascular endothelial ectonucleotidase, is responsible for the hydrolysis of both extracellular ATP and ADP in the blood plasma to AMP. Studies were therefore conducted to evaluate the role of vascular NTPDase-1/cd39 in modulating platelet activation and vascular injury in cardiac xenografts. Cardiac xenografts from both wild-type and cd39 knockout mice (C57BL/6 x 129 Svj) were transplanted into Lewis rats. Alterations in cd39 mRNA transcripts and NTPDase activity expression were evaluated in wild-type grafts in untreated rats and then following complement depletion and immunosuppression. Rejection responses were studied with both mutant and wild-type grafts in the following models: presensitization with or without complement depletion, complement depletion alone, and with chronic immunosuppression to induce long-term graft survival. NTPDase biochemical activity in wild-type xenografts rapidly decreased after transplantation but soon rebounded with graft survival. Elevated levels of cd39 mRNA with associated increases in NTPDase activity were observed in all long-term surviving wild-type grafts. Hyperacute xenograft rejection times were comparable in wild-type and mutant grafts but cd39-deficient grafts were subject to more rapid rejection and exhibited pronounced vascular injury in complement-depleted, presensitized rats. The cd39-deficient grafts in immunosuppressed recipients were subject to increased intravascular platelet sequestration and fibrin deposition; this resulted in focal myocardial infarction in long-term surviving mutant xenografts. Augmentation of NTPDase-1 activity may be an important adaptive response for graft survival. Our results suggest that NTPDase-1/cd39 influences pathways of vascular injury in cardiac xenografts.

Rupture of dissecting aneurysm in a China Airlines co-pilot

A 46-year-old male co-pilot of China Airlines developed shortness of breath during landing on a flight from Tokyo to Taipei on May 17, 1994. He was found dead shortly after landing. He was well and had passed his semi-annual health examination with no history of cardiovascular disease or hereditary disease. A dissecting aneurysm of DeBakey type I and cardiac tamponade with 200 ml blood inside the pericardial cavity during autopsy was noted. The right and left coronary arteries showed atherosclerotic changes with the lumen narrowing down to 30% in the anterior descending branch. Focal myocardial infarction with a healing scar, atheroma and arteriosclerosis of the small arteries including the kidney were observed. Nonspecific changes of the chest X-Ray and EKG with hyperlipoproteinemia suggests that a more advanced technique is required to carefully examine the heart condition during regular physical checkups to prevent sudden illness that might contribute to mass disaster.

Side effects of rapamycin in the rat.

The side effects of Rapamycin was evaluated by histopathological examination of the heart, kidneys, and eyes of treated Lewis rats. Rapamycin was administered during 14 days by continuous intravenous infusions at doses of 0.5, 1.0, and 1.5 mg/kg/day. Focal myocardial infarction was observed in three of five rats with Rapamycin given at 1.5 mg/kg/day and two of 22 rats with 1.0 mg/kg/day. There were no sign of myocardial toxicity at a Rapamycin dose of 0.5 mg/kg/day. The retina of one eye of a rat treated at a dose of 1.5 mg/kg/day had a small area of focal ischemic necrosis. The kidneys were normal at all doses.

Transformation of small focal myocardial infarction into transmural

The widespread classification of coronary heart disease does not accidentally distinguish two forms of myocardial infarction - large-focal and small-focal. These forms also require appropriate treatment tactics. Many years of clinical experience have created the idea of milder course and favorable prognosis of small focal myocardial infarction, but from time to time there are reports, forcing to reconsider its attitude due to propensity of this form to recurrence, unpredictable frequent exacerbation and even worse prognosis.

Vanillylmindalic acid excretion in patients with coronary heart disease

Daily urinary excretion of vanillylmindalic acid in patients with acute myocardial infarction and progressive angina pectoris was studied in dynamics. We examined 110 patients on days 1-5, 6-10, 30-35 of the disease (group I). There were 76 men, aged 32-84 years (mean age, 56.0), and 34 women, aged 44-85 years (mean age, 66.3). Large focal myocardial infarction was diagnosed in 69 (62.7%) patients, small focal - in 18 (16.4%), recurrent - in 23 (20.9%). Myocardial infarction of anterior wall of the left ventricle was diagnosed in 64 patients, posterior - in 32 patients, and anteroposterior - in 14 patients. Acute period of the disease occurred in 66 (60%) patients with various complications: cardiac rhythm and conduction disorders, circulatory disorders, pulmonary edema, 1st-II degree cardiogenic shock, thromboembolism, acute atony of the stomach and intestines, cardiac asthma.

Study of acoustic cardiac symptomatology in patients with acute myocardial infarction

The main objective of this study was to study I and II heart tones using phono- and spectrography in healthy subjects and in patients with acute myocardial infarction. We examined 79 patients (59 men and 20 women) with acute transmural large focal myocardial infarction aged 30 to 77 years. The diagnosis of acute myocardial infarction was made on the basis of clinical, electrocardiographic and laboratory studies.

Radioautographic studies in experimental myocardial infarction: Profiles of ischemic blood flow and quantification of infarct size in relation to magnitude of ischemic zone

A radioautographic method was adapted to assess regional blood flow in focal myocardial infarction produced experimentally in dogs with ligation of a branch of the left circumflex artery. Twenty-four hours later, the dogs were given an infusion of 1 millicurie of 14C-antlpyrine and killed. Radloautograms were prepared from 20 μ full thickness sections Of the infarcted segment of each left ventricle. Adjacent tissue sections were also prepared for histopathologic study and comparison. Photodensltometric scanning of radioautograms in transverse and transmural planes permitted quantification of regional blood flow, measurement of dimensions of the zones of blood flow reduction and construction of profiles of Ischemic blood flow within a cubic reference system. Thus, transverse plane scans showed symmetric profiles of decreasing blood flow from each normal margin (mean ± standard error of the mean 0.75 ± 0.11 ml/ g per min) to the center of the Infarct (mean 0.08 ± 0.02 ml/ g per min or 11.7 ± 3.5 percent of normal flow); transmural plane scans showed an asymmetric profile of decreasing blood flow from the epicardlum (mean 0.36 ± 0.06 ml/ g per min) to the center of the infarct and a subsequent increase to 0.22 ± 0.03 ml/ g per min near the endocardial surface. From a comparative analysis of radioautograms with corresponding adjacent histologie sections we determined that (1) myocardial necrosis was first evident at the point of blood flow reduction that averaged 45.2 ± 3.2 percent of normal values; (2) a border zone of intermediate flow reduction where cell viability was maintained 24 hours after infarction averaged 4.5 ± 0.5 mm and encompassed 30.4 ± 3.0 percent of total ischemic zone width; and (3) on the basis of various geometric models, the size of the myocardial infarct in these experiments was approximately 40 percent of that of the ischemic zone.