Effects of a 980 nm Diode Laser as an Adjunct to Nonsurgical Periodontal Therapy on Periodontal Status and Inflammatory Markers in Patients After Myocardial Infarction: A Randomized Controlled Trial.

Objective: The aim of this study was to evaluate the efficacy of diode laser (DL) therapy as an adjunct to nonsurgical periodontal therapy in the treatment of periodontitis in patients after myocardial infarction (MI). Methods: After given permission by Ethics Commission of the Pomeranian Medical University (KB-0012/06/12), 36 patients <65 years of age (mean: 56.3 ± 7.9) with periodontitis, 6 weeks to 6 months after MI were enrolled for the study. The control group (n = 18) received nonsurgical periodontal therapy, whereas the test group (n = 18) received nonsurgical periodontal therapy followed by laser therapy of the periodontal pockets with 980 nm DL, 1 W, continuous wave mode, and 20 sec per tooth side. Procedures were repeated twice at 5-7 day intervals. Clinical periodontal parameters and inflammatory markers in gingival crevicular fluid (GCF) [elastase, aspartate transaminase (AST), alanine transaminase (ALT) and interleukin (IL)-6, proteins], bloodstream [fibrinogen, high-sensitivity CRP (hs-CRP), IL-6, AST and ALT], and lipid fractions (triglycerides, high-density lipoprotein, low-density lipoprotein, and total cholesterol) were measured before treatment, 2 weeks, and 3 months after treatment. Results: The difference between groups in the reduction of periodontal pocket depth (PPD) in pockets ≥7 mm was found to be significant in the test group (p < 0.05). There was also a statistically significant reduction in the volume of GCF and hs-CRP concentration in blood 2 weeks after the completion of treatment in the test group (p < 0.05). Conclusions: Within the limits of this study, it can be concluded that in the nonsurgical treatment of periodontitis with patients after MI, the additional use of DL enables greater reduction of PPD in pockets ≥7 mm. In addition, a faster reduction of GCF volume and hs-CRP was noted in the laser group.

Photobiomodulation therapy's effects on cardiac fibrosis activation after experimental myocardial infarction.

INTRODUCTION: Ischemic heart disease is the leading cause of death worldwide, and interventions to reduce myocardial infarction (MI) complications are widely researched. Photobiomodulation therapy (PBMT) has altered multiple biological processes in tissues and organs, including the heart. OBJECTIVES: This study aimed to assess the temporal effects of PBMT on cardiac fibrosis activation after MI in rats. In this proof-of-concept study, we monitored the change in expression patterns over time of genes and microRNAs (miRNAs) involved in the formation of cardiac fibrosis post-MI submitted to PBMT. MATERIALS AND METHODS: Experimental MI was induced, and PBMT was applied shortly after coronary artery ligation (laser light of wavelength 660 nm, 15 mW of power, energy density 22.5 J/cm2 , 60 seconds of application, irradiated area 0.785 cm2 , fluence 1.1 J/cm2 ). Ventricular septal samples were collected at 30 minutes, 3, 6, 24 hours, and 3 days post-MI to determine temporal PBMT's effects on messenger RNA (mRNA) expression associated with cardiac fibrosis activation and miRNAs expression. RESULTS: PBMT, when applied after ischemia, reversed the changes in mRNA expression of myocardial extracellular matrix genes induced by MI. Surprisingly, PBMT modified cardiac miRNAs expression related to fibrosis replacement in the myocardium. Expression correlations between myocardial mRNAs were assessed. The correlation coefficient between miRNAs and target mRNAs was also determined. A positive correlation was detected among miR-21 and transforming growth factor beta-1 mRNA. The miR-29a expression negatively correlated to Col1a1, Col3a1, and MMP-2 mRNA expressions. In addition, we observed that miR-133 and Col1a1 mRNA were negatively correlated. CONCLUSION: The results suggest that PBMT, through the modulation of gene transcription and miRNA expressions, can interfere in cardiac fibrosis activation after MI, mainly reversing the signaling pathway of profibrotic genes.

Colchicine treatment early after infarction attenuates myocardial inflammatory response demonstrated by 14C-methionine imaging and subsequent ventricular remodeling by quantitative gated SPECT.

OBJECTIVE: Colchicine has been used as an anti-inflammatory agent and may be cardioprotective after acute myocardial infarction (AMI). We investigated how colchicine administration after AMI affects the myocardial inflammatory response using 14C-methionine and subsequent ventricular remodeling using single-photon emission computed tomography (SPECT) in a rat model of AMI. METHODS: The left coronary artery (LCA) was occluded for 30 min followed by reperfusion. 14C-methionine was injected at 20 min before sacrifice. The LCA was re-occluded at 1 min before sacrifice and 99mTc-methoxyisobutylisonitrile (99mTc-MIBI) was injected. Colchicine was administered intraperitoneally from day 1 to the day before 14C-methionine injection. Dual-tracer autoradiography of the left ventricular short-axis slices was performed. The methionine uptake ratio in an ischemic area was calculated. 99mTc-MIBI gated SPECT assessed end-diastolic volume (EDV), end-systolic volume (ESV) and left ventricular ejection fraction (LVEF). On Cluster of Differentiation 68 with 4',6-diamidino-2-phenylindole (CD68/DAPI) staining the positive myocardial cell percentage in an ischemic area was calculated. RESULTS: In control rats, 14C-methionine uptake ratios on day 3 and 7 were 1.87 ± 0.15 and 1.39 ± 0.12, respectively. With colchicine, the uptake was reduced on days 3 (1.56 ± 0.26, p = 0.042) and 7 (1.23 ± 0.10, p = 0.030). Colchicine treated rats showed smaller EDV, ESV, and higher LVEF compared with control rats. At 8 weeks, those in control rats were 864 ± 115 µL, 620 ± 100 µL, 28.4 ± 2.5%, and in colchicine rats 665 ± 75 µL, 390 ± 97 µL, 42.2 ± 8.5% (p = 0.012, 0.0061, 0.0083), respectively. In control rats, CD68/DAPI positive myocardial cell percentages on days 3 and 7 were 38.4 ± 1.9% and 24.0 ± 2.4%, respectively. With colchicine, the percentages were reduced significantly on both days 3 (31.5 ± 2.0%, p < 0.0001) and 7 (12.0 ± 1.6%, p < 0.0001) as compared with the control. CONCLUSIONS: Short-term colchicine treatment after AMI attenuated the post-AMI inflammatory response and subsequent ventricular remodeling and dysfunction. 14C-methionine imaging and gated 99mTc-MIBI SPECT would be feasible to monitor the effectiveness of anti-inflammatory therapy and left ventricular function.

Noninvasive light emitting diode therapy: A novel approach for postinfarction ventricular arrhythmias and neuroimmune modulation.

BACKGROUND: Sympathetic neural activation plays a key role in the incidence and maintenance of acute myocardial infarction (AMI) induced ventricular arrhythmia (VA). Furthermore, previous studies showed that AMI might induce microglia and sympathetic activation and that microglial activation might contribute to sympathetic activation. Recently, studies showed that light emitting diode (LED) therapy might attenuate microglial activation. Therefore, we hypothesized that LED therapy might reduce AMI-induced VA by attenuating microglia and sympathetic activation. METHODS: Thirty anesthetized rats were randomly divided into three groups: the Control group (n = 6), AMI group (n = 12), and AMI + LED group (n = 12). Electrocardiogram (ECG) and left stellate ganglion (LSG) neural activity were continuously recorded. The incidence of VAs was recorded during the first hour after AMI. Furthermore, we sampled the brain and myocardium tissue of the different groups to examine the microglial activation and expression of nerve growth factor (NGF), interleukin-18 (IL-18), and IL-1ß, respectively. RESULTS: Compared to the AMI group, LED therapy significantly reduced the incidence of AMI-induced VAs (ventricular premature beats [VPB] number: 85.08 ± 13.91 vs 27.5 ± 9.168, P < .01; nonsustained ventricular tachycardia (nSVT) duration: 34.39 ± 8.562 vs 9.005 ± 3.442, P < .05; nSVT number: 18.92 ± 4.52 vs 7.583 ± 3.019, P < .05; incidence rate of SVT/VF: 58.33% vs. 8.33%, P < .05) and reduced the LSG neural activity (P < .01) in the AMI + LED group. Furthermore, LED significantly attenuated microglial activation and reduced IL-18, IL-1ß, and NGF expression in the peri-infarct myocardium. CONCLUSION: LED therapy may protect against AMI-induced VAs by suppressing sympathetic neural activity and the inflammatory response.

Association between radiation heart dosimetric parameters, myocardial infarct and overall survival in stage 3 non-small cell lung cancer treated with definitive thoracic radiotherapy.

OBJECTIVES: The aim of this retrospective observational study is to assess the association between various radiation heart dosimetric parameters (RHDPs) and acute myocardial infarct (AMI) and overall survival (OS) outcomes in stage III non-small cell lung cancer (NSCLC) treated with definitive radiotherapy with or without chemotherapy. MATERIALS AND METHODS: We identified eligible patients treated at two institutions from 2007 to 2014. We linked their electronic medical records to the national AMI and death registries. We performed univariable and multivariable Cox regressions analysis to assess the association between various RHDPs, AMI and OS. RESULTS: 120 eligible patients were included with a median follow-up of 17.6 months. Median age was 65.5 years. Median prescription dose was 60 Gy. Median mean heart dose (MHD) was 12.6 Gy. Univariable analysis showed that higher MHD (hazard ratio (HR), 1.03; 95% confidence interval (CI), 1.01-1.06; P = .008) and volume of heart receiving at least 5 Gy (V5) (HR, 1.01; 95% CI, 1.00-1.03; P = .042) were associated with increased hazards for AMI. Univariable analysis showed that higher MHD, V5, V25, V30, V40, V50 and dose to 30% of heart volume were associated with increased hazards for death. Multivariable analysis showed that there was no statistically significant association between various RHDPs and OS. CONCLUSION: The incidence of AMI is low among stage III NSCLC treated with definitive radiotherapy with or without chemotherapy. There is insufficient evidence to conclude that RHDPs are associated with AMI or OS in our study.

Effect of low-level laser-treated mesenchymal stem cells on myocardial infarction.

Cardiovascular disease is the leading cause of death worldwide. Although cardiac transplantation is considered the most effective therapy for end-stage cardiac diseases, it is limited by the availability of matching donors and the complications of the immune suppressive regimen used to prevent graft rejection. Application of stem cell therapy in experimental animal models was shown to reverse cardiac remodeling, attenuate cardiac fibrosis, improve heart functions, and stimulate angiogenesis. The efficacy of stem cell therapy can be amplified by low-level laser radiation. It is well established that the bio-stimulatory effect of low-level laser is influenced by the following parameters: wavelength, power density, duration, energy density, delivery time, and the type of irradiated target. In this review, we evaluate the available experimental data on treatment of myocardial infarction using low-level laser. Eligible papers were characterized as in vivo experimental studies that evaluated the use of low-level laser therapy on stem cells in order to attenuate myocardial infarction. The following descriptors were used separately and in combination: laser therapy, low-level laser, low-power laser, stem cell, and myocardial infarction. The assessed low-level laser parameters were wavelength (635-804 nm), power density (6-50 mW/cm2), duration (20-150 s), energy density (0.96-1 J/cm2), delivery time (20 min-3 weeks after myocardial infarction), and the type of irradiated target (bone marrow or in vitro-cultured bone marrow mesenchymal stem cells). The analysis focused on the cardioprotective effect of this form of therapy, the attenuation of scar tissue, and the enhancement of angiogenesis as primary targets. Other effects such as cell survival, cell differentiation, and homing are also included. Among the evaluated protocols using different parameters, the best outcome for treating myocardial infarction was achieved by treating the bone marrow by one dose of low-level laser with 804 nm wavelength and 1 J/cm2 energy density within 4 h of the infarction. This approach increased stem cell survival, proliferation, and homing. It has also decreased the infarct size and cell apoptosis, leading to enhanced heart functions. These effects were stable for 6 weeks. However, more studies are still required to assess the effects of low-level laser on the genetic makeup of the cell, the nuclei, and the mitochondria of mesenchymal stromal cells (MSCs).

Inducibility of Ventricular Arrhythmia 1 Year Following Treatment with Heavy Ion Irradiation in Dogs with Myocardial Infarction.

BACKGROUND: Targeted external heavy ion irradiation (THIR) of rabbit hearts 2 weeks after myocardial infarction (MI) reduced the vulnerability of fatal ventricular tachyarrhythmias (VT/VF) in association with the increased connexin43 (Cx43). Increased Cx43 was maintained for at least 1 year in normal rabbits, but the long-term antiarrhythmic effects in the MI model are unknown. We investigated the propensity for late potentials and VT/VF inducibility. METHODS: Intracoronary injection of microspheres was performed to induce nontransmural MI in anesthetized eight beagles. Four beagles were treated with THIR (12 C6+ , 15 Gy) 2 weeks later (MI + THIR group), and four without THIR served as controls (MI group). Signal-averaged electrocardiography, programmed electrical stimulation, immunohistochemical analysis, and echocardiograms were performed at 1 year. RESULTS: Filtered QRS duration was exacerbated after MI and remained unchanged for 1 year in the MI group (118 ± 1.4 ms), but significantly returned toward baseline in the MI + THIR group (109 ± 6.9 ms). Similarly, root mean square voltage of the last 40 ms was exacerbated after MI, but recovered after THIR. VT/VF inducibility decreased to 25% in the MI + THIR group compared with 100% in the MI group. Immunostaining Cx43 expression in cardiac tissues significantly increased by 24-45% in the MI + THIR group. Left ventricular ejection fractions remained within the normal range in both groups. CONCLUSION: A single exposure of the dog heart to 12 C irradiation attenuated vulnerability to ventricular arrhythmia after the induction of MI for at least 1 year through the modulation of Cx43 expression.

Maximal oxygen uptake and exercise tolerance are improved in rats with heart failure subjected to low-level laser therapy associated with resistance training.

Exercise tolerance and maximal oxygen uptake (VO2max) are reduced in heart failure (HF). The influence of combined resistance training (RT) and low-level laser therapy (LLLT) on exercise tolerance and VO2max in HF has not yet been explored. The aim of this study was to evaluate the influence of combined RT and LLLT on VO2max and exercise tolerance in rats with HF induced by myocardial infarction (MI). Rats were allocated to sedentary sham (Sed-Sham, n = 12), sedentary heart failure (Sed-HF, n = 9), RT heart failure (RT-HF, n = 7) and RT associated with LLLT heart failure (RT + LLLT-HF, n = 7) groups. After MI or sham surgery, rats underwent a RT and LLLT protocol (applied immediately after RT) for 8 weeks. VO2max and exercise tolerance were evaluated at the end of protocol. HF rats subjected to LLLT combined with RT showed higher VO2basal (41 %), VO2max (40 %), VO2reserve (39 %), run distance (46 %), time to exhaustion (30 %) and maximal velocity (22 %) compared with HF rats that underwent RT alone. LLLT associated with RT improved oxygen uptake and exercise tolerance compared with RT alone in HF rats.

Low-Level Laser Irradiation Precondition for Cardiac Regenerative Therapy.

OBJECTIVE: The purpose of this article was to review the molecular mechanisms of low-level laser irradiation (LLLI) preconditioning for heart cell therapy. BACKGROUND DATA: Stem cell transplantation appears to offer a better alternative to cardiac regenerative therapy. Previous studies have confirmed that the application of LLLI plays a positive role in regulating stem cell proliferation and in remodeling the hostile milieu of infarcted myocardium. Greater understanding of LLLI's underlying mechanisms would be helpful in translating cell transplantation therapy into the clinic. METHODS: Studies investigating LLLI preconditioning for cardiac regenerative therapy published up to 2015 were retrieved from library sources and Pubmed databases. RESULTS: LLLI preconditioning stimulates proliferation and differentiation of stem cells through activation of cell proliferation signaling pathways and alteration of microRNA expression. It also could stimulate paracrine secretion of stem cells and alter cardiac cytokine expression in infarcted myocardium. CONCLUSIONS: LLLI preconditioning provides a promising approach to maximize the efficacy of cardiac cell-based therapy. Although many studies have reported possible molecular mechanisms involved in LLLI preconditioning, the exact mechanisms are still not clearly understood.

Low-Level Laser Therapy to the Bone Marrow Reduces Scarring and Improves Heart Function Post-Acute Myocardial Infarction in the Pig.

OBJECTIVE: Cell therapy for myocardial repair is one of the most intensely investigated strategies for treating acute myocardial infarction (MI). The aim of the present study was to determine whether low-level laser therapy (LLLT) application to stem cells in the bone marrow (BM) could affect the infarcted porcine heart and reduce scarring following MI. METHODS: MI was induced in farm pigs by percutaneous balloon inflation in the left coronary artery for 90 min. Laser was applied to the tibia and iliac bones 30 min, and 2 and 7 days post-induction of MI. Pigs were euthanized 90 days post-MI. The extent of scarring was analyzed by histology and MRI, and heart function was analyzed by echocardiography. RESULTS: The number of c-kit+ cells (stem cells) in the circulating blood of the laser-treated (LT) pigs was 2.62- and 2.4-fold higher than in the non-laser-treated (NLT) pigs 24 and 48 h post-MI, respectively. The infarct size [% of scar tissue out of the left ventricle (LV) volume as measured from histology] in the LT pigs was 3.2 ± 0.82%, significantly lower, 68% (p < 0.05), than that (16.6 ± 3.7%) in the NLT pigs. The mean density of small blood vessels in the infarcted area was significantly higher [6.5-fold (p < 0.025)], in the LT pigs than in the NLT ones. Echocardiography (ECHO) analysis for heart function revealed the left ventricular ejection fraction in the LT pigs to be significantly higher than in the NLT ones. CONCLUSIONS: LLLT application to BM in the porcine model for MI caused a significant reduction in scarring, enhanced angiogenesis and functional improvement both in the acute and long term phase post-MI.

A rare case of cisplatin-induced acute myocardial infarction in a patient receiving chemoradiation for lung cancer.

We present this unusual case of cisplatin-induced acute myocardial infarction in a patient with no organic coronary artery disease (CAD), receiving chemoradiation for small cell lung cancer. Patient developed symptoms of acute coronary syndrome after receiving two cycles of cisplatin and etoposide. The possible mechanism of vasospasm induced by cisplatin, in the background of thoracic radiation and hypomagnesemia, is discussed in this case report.

Amelioration of cardiac function and activation of anti-inflammatory vasoactive peptides expression in the rat myocardium by low level laser therapy.

Low-level laser therapy (LLLT) has been used as an anti-inflammatory treatment in several disease conditions, even when inflammation is a secondary consequence, such as in myocardial infarction (MI). However, the mechanism by which LLLT is able to protect the remaining myocardium remains unclear. The present study tested the hypothesis that LLLT reduces inflammation after acute MI in female rats and ameliorates cardiac function. The potential participation of the Renin-Angiotensin System (RAS) and Kallikrein-Kinin System (KKS) vasoactive peptides was also evaluated. LLLT treatment effectively reduced MI size, attenuated the systolic dysfunction after MI, and decreased the myocardial mRNA expression of interleukin-1 beta and interleukin-6 in comparison to the non-irradiated rat tissue. In addition, LLLT treatment increased protein and mRNA levels of the Mas receptor, the mRNA expression of kinin B2 receptors and the circulating levels of plasma kallikrein compared to non-treated post-MI rats. On the other hand, the kinin B1 receptor mRNA expression decreased after LLLT. No significant changes were found in the expression of vascular endothelial growth factor (VEGF) in the myocardial remote area between laser-irradiated and non-irradiated post-MI rats. Capillaries density also remained similar between these two experimental groups. The mRNA expression of the inducible nitric oxide synthase (iNOS) was increased three days after MI, however, this effect was blunted by LLLT. Moreover, endothelial NOS mRNA content increased after LLLT. Plasma nitric oxide metabolites (NOx) concentration was increased three days after MI in non-treated rats and increased even further by LLLT treatment. Our data suggest that LLLT diminishes the acute inflammation in the myocardium, reduces infarct size and attenuates left ventricle dysfunction post-MI and increases vasoactive peptides expression and nitric oxide (NO) generation.

Induction of autologous mesenchymal stem cells in the bone marrow by low-level laser therapy has profound beneficial effects on the infarcted rat heart.

BACKGROUND AND OBJECTIVES: The adult mammalian heart is known to have a very limited regenerative capacity following acute ischemia. In this study we investigated the hypothesis that photobiostimulation of autologous bone-marrow-derived mesenchymal stem cells (MSCs) by low-level laser therapy (LLLT) applied to the bone marrow (BM), may migrate to the infarcted area and thus attenuate the scarring processes following myocardial infarction (MI). MATERIALS AND METHODS: Sprague-Dawley rats underwent experimental MI. LLLT (Ga-Al-As diode laser, power density 10 mW/cm², for 100 seconds) was then applied to the BM of the exposed tibia at different time intervals post-MI (20 minutes and 4 hours). Sham-operated infarcted rats served as control. RESULTS: Infarct size and ventricular dilatation were significantly reduced (76% and 75%, respectively) in the laser-treated rats 20 minutes post-MI as compared to the control-non-treated rats at 3 weeks post-MI. There was also a significant 25-fold increase in cell density of c-kit+ cells in the infarcted area of the laser-treated rats (20 minutes post-MI) as compared to the non-laser-treated controls. CONCLUSION: The application of LLLT to autologous BM of rats post-MI offers a novel approach to induce BM-derived MSCs, which are consequently recruited from the circulation to the infarcted heart and markedly attenuate the scarring process post-MI.

Congenital giant aneurysm of the left coronary artery.

We report an unusual case of congenital giant coronary aneurysm. A 23 year-old male with a history of acute myocardial infarction presented an abnormal shadow in the left cardiac border on routine X-ray. Electrocardiogram and physical examination were normal without any clinical signs of inflammation, but computed tomography (CT) scan and cardiac magnetic resonance imaging (MRI) revealed a giant (>50mm) coronary aneurysm. Coronary artery bypass grafting (CABG) with coronary artery aneurysm (CAA) resection resolved the CAA. Coronary artery aneurysms are entities of localised dilation and can be common events in chronic infectious disease as a result of the systemic inflammatory state; however, giant coronary aneurysms (measuring more than 50mm) are rare. This is especially true where the pathological aetiology was not clearly defined or was believed to be of congenital origin. To date only a few published case reports exist for this type of pathological entity.

Low-level laser irradiation alters cardiac cytokine expression following acute myocardial infarction: a potential mechanism for laser therapy.

OBJECTIVES: Low-level laser irradiation (LLLI) has the potential of exerting cardioprotective effect following myocardial infarction (MI). The authors hypothesized that LLLI could influence the expression of cardiac cytokines and contribute to the reversal of ventricular remodeling. BACKGROUND: LLLI regulates the expression of cytokines after tissue damage. However, little is known concerning the alteration of the cardiac cytokine expression profile after LLLI. METHODS: MI was created by coronary ligation. The surviving rats were divided randomly into laser and control groups. 33 rats were exposed to a diode laser (635 nm, 5 mW, CW, laser, beam spot size 0.8 cm(2), 6 mW/cm(2), 150 sec, 0.8 J, 1J/cm(2)) as laser group. Another 33 rats received only coronary ligation and served as control group. 28 rats received a thoracotomy without coronary ligation (sham group). One day after laser irradiation, 5 rats from each group were sacrificed and the heart tissues were analyzed by cytokine antibody arrays. Enzyme-linked immunosorbent assay (ELISA) was performed to confirm its reliability. Two weeks after MI, cardiac function and structure were evaluated by echocardiography and histological study. RESULTS: Cytokine antibody array indicated 4 cytokines were significantly changed after laser therapy. ELISA confirmed that granulocyte-macrophage colony stimulating factor and fractalkine were the cytokines involved in the response to therapeutic laser irradiation. However, there was no difference in cytokine release between various groups at 2 weeks after MI. Although LLLI did not improve the damaged heart function, it did reduce the infarct area expansion. CONCLUSIONS: The antibody-based protein array technology was applied for screening the cytokine expression profile following MI, with or without laser irradiation. The expression of multiple cytokines was regulated in the acute phase after LLLI. Our results revealed a potential novel mechanism for applying laser therapy to the treatment of heart disease.

Insuficiencia mitral isquémica: utilidad de la ecocardiografía en su evaluación y tratamiento / Ischemic mitral regurgitation: utility of echocardiography in evaluation and treatment

La regurgitación mitral isquémica (RMI) es una complicación común de la enfermedad arterial coronaria que produce insuficiencia cardíaca en un alto porcentaje de pacientes. Puede presentarse como una verdadera emergencia cuando es causada por un infarto del miocardio con ruptura del músculo papilar asociada a shock cardiogénico. La insuficiencia mitral isquémica crónica es una complicación frecuente trasel infarto agudo del miocardio, aparece aproximadamente en 20% de los casos y es mucho más probable en el infarto agudo del miocardio de localización inferior (38%) que en el anterior (10%). Es producida por una integración de varios mecanismos que influyen en su desarrollo y que básicamente están relacionados con remodelado local o global del ventrículo izquierdo, con disfunción y disincronía del mismo. Su evaluación adecuada y rápida puede influir en el éxito de su tratamiento y en el mejor pronóstico de los pacientes. Una indicación quirúrgica precoz, actuando sobre ventrículos menos remodelados, y la innovación en el arsenal de dispositivos y técnicas quirúrgicas permitirán una corrección exitosa y duradera con baja mortalidad hospitalaria. En este sentido, las nuevas exploraciones desarrolladas por la ecocardiografía han adquirido una gran importancia al permitir evaluar la severidad de la insuficiencia mitral, el grado de disfunción local o global del ventrículo izquierdo y el estado del aparato valvular mitral lo que ha hecho del método la exploración más confiable y necesaria en estos pacientes. Revisamos la utilidad y el papel del ecocardiograma en el estudio de la insuficienciamitral isquémica.

Ischemic mitral regurgitation is a common complication of coronary heart disease that leads to heart failure in a high percentage of patients. It can present as a real emergency when it is caused by a myocardial infarction with rupture of a papillary muscle resulting in cardiogenic shock. Chronic ischemic mitral regurgitation is a frequent complication after a myocardial infarction in 20% of cases and it is even more frequent when the myocardial infarction is localized in the inferior wall (38%) than the anterior wall (10%). This complication is the result of the interaction of several mechanisms that are related to local or global remodeling of the left ventricle and associated left ventricle dysfunction and desynchronization. Prompt and precise evaluation can be of vital importance for successful treatment and a better prognosis. Early surgery in less remodeled ventricles, and innovation in devices and surgical techniques will lead to long-lasting successful correction with low in-hospital mortality. Therefore, new developments in echocardiography have acquired substantial significance for the evaluation of the severity of mitral insufficiency, the grade of local or global dysfunction of the left ventricle and the state of the mitral valve apparatus, rendering this method more reliable and indispensable for these patients. We reviewed the utility and role of echocardiography in the evaluation ofischemic mitral regurgitation.

Pulsed magnetic field induces angiogenesis and improves cardiac function of surgically induced infarcted myocardium in Sprague-Dawley rats.

OBJECTIVE: It was the aim of this study to investigate the impact of pulsed magnetic field (PMF) on ischemic myocardium, though it has been reported that PMF treatment is a safe and effective method to facilitate bone and cutaneous wound healing. METHODS: In this report, we describe a study in which 10 Hz 4 mT PMF and 15 Hz 6 mT PMF was used to treat rats with myocardial infarction (MI). RESULTS: After 28 days of treatment, the rats treated with 15 Hz 6 mT PMF exhibited decreased left ventricular end-diastolic pressure and accelerated maximum dp/dt of left ventricular pressure when compared with the untreated MI and the MI + 10 Hz 4 mT groups. Additionally, capillary density was increased and infarction area size was decreased in the MI + 15 Hz 6 mT group. Furthermore, the plasma vascular endothelial growth factor concentration and the protein expression of vascular endothelial growth factor receptor 2 in myocardial tissue were increased in rats of the MI + 15 Hz 6 mT group. CONCLUSION: This study shows that 15 Hz 6 mT PMF promotes myocardial angiogenesis and improves cardiac function after MI in rats. This suggests that there is a potential use for some PMF signal strengths in ischemic myocardial disease.

Sympathetic excitation during exercise as a cause of attenuated heart rate recovery in patients with myocardial infarction.

BACKGROUND: Heart rate recovery (HRR) after exercise is known as a predictor of cardiac death in patients with heart disease. The mechanism is not fully understood, although a parasympathetic mechanism has been reported. To elucidate the factors that influence HRR, we evaluated the relationship of HRR with exercise performance and plasma norepinephrine (NE), lactic acid and B-type natriuretic peptide (BNP) responses to exercise testing. METHODS: The study population consisted of 52 male patients (age 58 +/- 9.6 years) who had experienced myocardial infarction without residual ischemia, uncompensated heart failure or atrial fibrillation. All subjects underwent a symptom-limited cardiopulmonary exercise test without a cool-down period and echocardiography. NE, lactic acid and BNP were measured at rest and at peak exercise. RESULTS: HRR did not correlate with the left ventricular ejection fraction, peak VO(2), lactic acid and BNP. HRR significantly correlated with the increment in heart rate (HR) from rest to peak exercise (DeltaHR) (r=0.30, p<0.05). When we divided DeltaHR into two phases at the anaerobic threshold (AT), HRR significantly correlated with DeltaHR (peak-AT) (r=0.409, p<0.01), but not with DeltaHR (AT-rest). There was a significant negative correlation between HRR and NE both at rest and at peak exercise (r=-0.286, p<0.05, r=-0.310, p<0.05). HRR was also correlated significantly with DeltaHR/logDeltaNE as an index of sensitivity to NE (r=0.421, p<0.01). Based on multiple regression analysis, DeltaHR and logDeltaNE predicted HRR (R(2)=0.467, p=0.0027). CONCLUSIONS: Present findings suggest that enhanced sympathetic excitation at maximum exercise suppresses parasympathetic reactivation and results in attenuation of HRR.

Extracorporeal cardiac shock wave therapy improves left ventricular remodeling after acute myocardial infarction in pigs.

OBJECTIVE: We have recently demonstrated that low-energy extracorporeal shock wave therapy improves chronic myocardial ischemia in pigs and humans. In this study, we examined whether our shock wave therapy is also effective at improving left ventricular remodeling after acute myocardial infarction in pigs. METHODS: Acute myocardial infarction was created by surgically excising the proximal segment of the left circumflex coronary artery (n=20). In the early treatment protocol, the shock wave therapy was started 3 days after acute myocardial infarction, whereas in the late treatment protocol, the therapy was started 4 weeks after acute myocardial infarction (n=5 each). The remaining animals were treated in the same manner, but without the shock wave treatment in each protocol (n=5 each). RESULTS: In the early treatment protocol, left ventricular ejection fraction was higher (42+/-1 vs. 32+/-1%, P<0.001) and left ventricular end-diastolic volume was smaller (95+/-1 vs. 99+/-2 ml, P<0.05) in the shock wave group compared with the control group. Furthermore, wall thickening fraction (32+/-1 vs. 28+/-1%, P<0.01), regional myocardial blood flow (1.7+/-0.2 vs. 1.0+/-0.1 ml/min/g, P<0.01), and number of capillaries in the border zone (1348+/-15 vs. 938+/-34 mm2, P<0.0001) were all significantly improved in the shock wave group compared with the control group. By contrast, in the late treatment group, no such beneficial effects of the shock wave therapy were noted. CONCLUSION: These results suggest that our extracorporeal cardiac shock wave therapy is also an effective and noninvasive therapy for improving left ventricular remodeling after acute myocardial infarction when started in the early phase of the disorder.