Estudos sobre thrombose cardiaca e endocardite parietal de origem não valvular

1.-Since the parietal endocarditis represents a chapter generally neglected, owing to the relative lack of cases, and somewhat confused because there various terms have been applied to a very same morbid condition, it justifies the work which previously we tried to accomplish, of nosographic classification. Taking into account the functional disturbances and the anatomical changes, all cases of parietal endocarditis referred to in the litterature were distributed by the following groups: A-Group-Valvulo-parietal endocarditis. 1st . type-Valvulo-parietal endocarditis per continuum. 2nd. type-Metastatic valvulo-parietal endocarditis. 3rd. type-Valvulo-parietal endocarditis of the mitral stenosis. B-Group-Genuine parietal endocarditis. a) with primary lesions in the myocardium. b) with primary lesions in the endocardium. 4th type-Fibrous chronic parietal endocarditis (B A Ü M L E R), « endocarditis parietalis simplex». 5th type-Septic acute parietal endocarditis (LESCHKE), «endocarditis parietalis septica». 6th type-Subacute parietal endocarditis (MAGARINOS TORRES), «endocarditis muralis lenta». 2.-Studying a group of 14 cases of fibrous endomyocarditis with formation of thrombi, and carrying together pathological and bacteriological examinations it has been found that some of such cases represent an infectious parietal endocarditis, sometimes post-puerperal, of subacute or slow course, the endocardic vegetations being contamined by pathogenic microörganisms of which the most frequent is the Diplococcus pneumoniae, in most cases of attenuated virulence. Along with the infectious parietal endocarditis, there occur arterial and venous thromboses (abdominal aorta, common illiac and femural arteries and external jugular veins). The case 5,120 is a typical one of this condition which we name subacute parietal endocarditis (endocarditis parietalis s. muralis lenta). 3.-The endocarditis muralis lenta encloses an affection reputed to be of rare occurrence, the «myocardite subaigüe primitive», of which JOSSERAND and GALLAVARDIN published in 1901 the first cases, and ROQUE and LEVY, another, in 1914. The «myocardite subaigüe primitive» was, wrongly, in our opinion, included by WALZER in the syndrome of myocardia of LAUBRY and WALZER, considering that, in the refered cases of JOSSERAND and GALLAVARDIN and in that of ROQUE and LEVY, there are described rather considerable inflammatory changes in the myocardium and endocardium. The designation «myocardia» was however especially created by LAUBRY and WALZER for the cases of heart failure in which the most careful aetiologic inquiries and the most minucious clinical examination were unable to explain, and in which, yet, the post-mortem examination did not reveal any anatomical change at all, it being forcible to admit, then, a primary functional change of the cardiac muscle fibre. This special cardiac condition is thoroughly exemplified in the observation that WALZER reproduces on pages 1 to 7 of his book. 4.-The clinical picture of the subacute parietal endocarditis is that of heart failure with oedemas, effusion in the serous cavities and passive chronic congestion of the lungs, liver, kideys and spleen associated, to that of an infectious disease of subacute course. The fever is rather transient oscillating around 99.5 F., being intersected with apyretic periods of irregular duration; it is not dependent on any evident extracardiac septic infection. In other cases the fever is slight, particularly in the final stage of the disease, when the heart failure is well established. The rule is to observe then, hypothermy. The cardiac-vascular signs consist of enlargement of the cardiac dullness, smoothing of the cardiac sounds, absence of organic murmurs and accentuated and persistent tachycardia up to a certain point independent of fever. The galloprhythm is present, in most cases. The signs of the pulmonary infarct are rather expressed by the aspect of the sputum, which is foamy and blood-streaked than by the classic signs. Cerebral embolism was a terminal accident on various cases. Yet, in some of them, along with the signs of septicemia and of cardiac insufficiency, occurred vascular, arterial (abdominal aorta, common illiac and femurals arteries) and venous (extern jugular veins) thromboses. 5. The autopsy revealed an inflammatory process located on the parietal endocardium, accompanied by abundant formation of ancient and recent thrombi, being the apex of the left ventricle, the junction of the anterior wall of the same ventricle, with the interventricular septum, and the right auricular appendage, the usual seats of the inflammatory changes. The region of the left branch of HIS’ bundle is spared. The other changes found consist of fibrosis of the myocardium (healed infarcts and circumscribed interstitial myocarditis), of recent visceral infarcts chiefly in lungs, spleen and brain, of recent or old infarcts in the kidneys (embolic nephrocirrhosis) and in the spleen, and of vascular thromboses (abdominal aorta, common illiacs and femurals arteries and external jugular veins), aside from hydrothorax, hydroperitoneum, cutaneous oedema, chronic passive congestion of the liver, lungs, spleen and kidneys and slight ictericia. 6. In the subacute parietal endocarditis the primary lesions sometimes locate themselves at the myocardium, depending on the ischemic necrosis associated to the arteriosclerosis of the coronariae arteries, or on an specific myocarditis. Other times, the absence of these conditions is suggestive of a primary attack to the parietal endocardium which is then the primary seat of the lesions. It matters little whatever may be the initial pathogenic mechanism; once injured the parietal endocardium and there being settled the infectious injury, the endocarditis develops with peculiar clinical and anatomical characters of remarkable uniformity, constituting an anatomo-clinical syndrome. 7.-The histologic sections show that recent lesions…

Cardiac magnetic resonance imaging and computed tomography in ischemic cardiomyopathy: an update

Abstract Ischemic cardiomyopathy is one of the major health problems worldwide, representing a significant part of mortality in the general population nowadays. Cardiac magnetic resonance imaging (CMRI) and cardiac computed tomography (CCT) are noninvasive imaging methods that serve as useful tools in the diagnosis of coronary artery disease and may also help in screening individuals with risk factors for developing this illness. Technological developments of CMRI and CCT have contributed to the rise of several clinical indications of these imaging methods complementarily to other investigation methods, particularly in cases where they are inconclusive. In terms of accuracy, CMRI and CCT are similar to the other imaging methods, with few absolute contraindications and minimal risks of adverse side-effects. This fact strengthens these methods as powerful and safe tools in the management of patients. The present study is aimed at describing the role played by CMRI and CCT in the diagnosis of ischemic cardiomyopathies.

Avaliação da evolução da área das valvas mitral e tricúspide fetal com ultrassonografia tridimensional

OBJETIVO: avaliar as áreas das válvulas atrioventriculares (tricúspide e mitral) de fetos normais por meio da ultrassonografia tridimensional (US3D) utilizando o método STIC (spatiotemporal image correlation). MÉTODOS: realizou-se estudo de corte transversal com 141 mulheres entre a 18ª e a 33ª semana de gestação. As medidas dos volumes cardíacos foram obtidas por um transdutor volumétrico transabdominal acoplado ao aparelho Voluson 730 Expert. Utilizou-se como referência o plano de quatro câmaras com a ROI (região de interesse) posicionada a partir dos ventrículos, sendo a área das valvas delimitada manualmente. Para conhecer a correlação das áreas valvulares com a idade gestacional, foram construídos diagramas de dispersão e calculou-se o coeficiente de correlação de Pearson (r). Foram calculadas médias, medianas, desvios padrão (DP), valores máximo e mínimo. Para se determinar intervalos de referência das áreas valvulares em função da idade gestacional, seguiu-se o modelo de regressão linear simples, utilizando o método de Altman, com nível de significância de p<0,05. Para o cálculo da reprodutibilidade intraobservador, utilizou-se o coeficiente de correlação intraclasse (CCI) e o gráfico de Bland-Altman. RESULTADOS: as áreas valvulares tricúspide e mitral se correlacionaram com a idade gestacional (r=0,80 para a tricúspide e r=0,79 para a mitral), sendo que a média aumentou da válvula tricúspide e mitral, respectivamente, de 0,22±0,10 cm² e de 0,23±0,10 cm² na 18º semana para 0,92±0,29 cm² e para 1,08±0,41 cm² na 33º semana de gestação. A reprodutibilidade intraobservador resultou em CCI=0,993 (IC95% 0,987; 0,996), com diferença média de 0,01 cm² (DP±0,2 cm² e IC95%±0,4 cm²). CONCLUSÃO: intervalos de referência para a área das valvares mitral e tricúspide entre a 18ªe a 33ª semana de gestação foram determinados pela US3D e se mostraram altamente reprodutíveis.

Clinical evaluation of enalapril maleate and furosemide usage in dogs with degenerative myxomatous mitral valve, CHF functional class Ib

Degenerative myxomatous mitral valve (DMMV) is a heart disease of high incidence in small animal clinical medicine, affecting mainly older dogs and small breeds. Thus, a scientific investigation was performed in order to evaluate the clinical use of the medicines furosemide and enalapril maleate in dogs with this disease in CHF functional class Ib before and after the treatment was established. For this purpose 16 dogs with the given valve disease were used, separated into two groups: the first received furosemide (n=8) and the second received enalapril maleate (n=8) throughout 56 days. The dogs were evaluated in four stages (T0, T14, T28 and T56 day) in relation to clinical signs, hematological, biochemical and serum assessment, which included serum angiotensin converting enzyme (ACE) and aldosterone, as well as radiography, electrocardiography, Doppler-echocardiography and blood pressure. The results regarding the clinical, hematological and serum chemistry evaluations revealed no significant changes in both groups, but significant reductions in the values of ACE and aldosterone in the group receiving enalapril maleate were verified. The radiographic examination revealed reductions of VHS values and variable Pms wave of the electrocardiogram in both groups, but no changes in blood pressure values were identified. The echocardiogram showed a significant decrease of the variables LVDd/s in the studied groups and the FS% in animals that received only enalapril. Therefore, analysis of results showed that monotherapy based on enalapril maleate showed better efficiency of symptoms control in patients with CHF functional class Ib.

Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats

Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10-min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min), followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrated that such preconditioning protects against neuronal death in rats and gerbils submitted to a lethal (10 min) ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescence when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned to control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min) and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH) groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of plasma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperfusion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the preconditioning phenomenon.

Vascular changes after cardiopulmonary bypass and ischemic cardiac arrest: roles of nitric oxide synthase and cyclooxygenase

Cardiac surgery involving ischemic arrest and extracorporeal circulation is often associated with alterations in vascular reactivity and permeability due to changes in the expression and activity of isoforms of nitric oxide synthase and cyclooxygenase. These inflammatory changes may manifest as systemic hypotension, coronary spasm or contraction, myocardial failure, and dysfunction of the lungs, gut, brain and other organs. In addition, endothelial dysfunction may increase the occurrence of late cardiac events such as graft thrombosis and myocardial infarction. These vascular changes may lead to increased mortality and morbidity and markedly lengthen the time of hospitalization and cost of cardiac surgery. Developing a better understanding of the vascular changes operating through nitric oxide synthase and cyclooxygenase may improve the care and help decrease the cost of cardiovascular operations.

Implications of ischemic penumbra for the diagnosis of brain death

The data reviewed here suggest the possibility that a global reduction of blood supply to the whole brain or solely to the infratentorial structures down to the range of ischemic penumbra for several hours or a few days may lead to misdiagnosis of irreversible brain or brain stem damage in a subset of deeply comatose patients with cephalic areflexia. The following proposals are advanced: 1) the lack of any set of clinically detectable brain functions does not provide a safe diagnosis of brain or brain stem death; 2) apnea testing may induce irreversible brain damage and should be abandoned; 3) moderate hypothermia, antipyresis, prevention of arterial hypotension, and occasionally intra-arterial thrombolysis may contribute to good recovery of a possibly large subset of cases of brain injury currently regarded as irreversible; 4) confirmatory tests for brain death should not replace or delay the administration of potentially effective therapeutic measures; 5) in order to validate confirmatory tests, further research is needed to relate their results to specific levels of blood supply to the brain. The current criteria for the diagnosis of brain death should be revised.

A pulsatile flow model for in vitro quantitative evaluation of prosthetic valve regurgitation

A pulsatile pressure-flow model was developed for in vitro quantitative color Doppler flow mapping studies of valvular regurgitation. The flow through the system was generated by a piston which was driven by stepper motors controlled by a computer. The piston was connected to acrylic chambers designed to simulate "ventricular" and "atrial" heart chambers. Inside the "ventricular" chamber, a prosthetic heart valve was placed at the inflow connection with the "atrial" chamber while another prosthetic valve was positioned at the outflow connection with flexible tubes, elastic balloons and a reservoir arranged to mimic the peripheral circulation. The flow model was filled with a 0.25% corn starch/water suspension to improve Doppler imaging. A continuous flow pump transferred the liquid from the peripheral reservoir to another one connected to the "atrial" chamber. The dimensions of the flow model were designed to permit adequate imaging by Doppler echocardiography. Acoustic windows allowed placement of transducers distal and perpendicular to the valves, so that the ultrasound beam could be positioned parallel to the valvular flow. Strain-gauge and electromagnetic transducers were used for measurements of pressure and flow in different segments of the system. The flow model was also designed to fit different sizes and types of prosthetic valves. This pulsatile flow model was able to generate pressure and flow in the physiological human range, with independent adjustment of pulse duration and rate as well as of stroke volume. This model mimics flow profiles observed in patients with regurgitant prosthetic valves.

Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts

We evaluated the effects of angiotensin-(1-7) (Ang-(1-7)) on post-ischemic function in isolated hearts from adult male Wistar rats perfused according to the Langendorff technique. Local ischemia was induced by coronary ligation for 15 min. After ischemia, hearts were reperfused for 30 min. Addition of angiotensin II (Ang II) (0.20 nM, N = 10) or Ang-(1-7) (0.22 nM, N = 10) to the Krebs-Ringer perfusion solution (KRS) before the occlusion did not modify diastolic or systolic tension, heart rate or coronary flow (basal values for Ang-(1-7)-treated hearts: 0.72 ± 0.08 g, 10.50 ± 0.66 g, 216 ± 9 bpm, 5.78 ± 0.60 ml/min, respectively). During the period of occlusion, the coronary flow, heart rate and systolic tension decreased (values for Ang-(1-7)-treated hearts: 2.83 ± 0.24 ml/min, 186 ± 7 bpm, 6.95 ± 0.45 g, respectively). During reperfusion a further decrease in systolic tension was observed in control (4.95 ± 0.60 g) and Ang II-treated hearts (4.35 ± 0.62 g). However, in isolated hearts perfused with KRS containing Ang-(1-7) the further reduction of systolic tension during the reperfusion period was prevented (7.37 ± 0.68 g). The effect of Ang-(1-7) on the systolic tension was blocked by the selective Ang-(1-7) antagonist A-779 (2 nM, N = 9), by the bradykinin B2 antagonist HOE 140 (100 nM, N = 10), and by indomethacin pretreatment (5 mg/kg, ip, N = 8). Pretreatment with L-NAME (30 mg/kg, ip, N = 8) did not change the effect of Ang-(1-7) on systolic tension (6.85 ± 0.61 g). These results show that Ang-(1-7) at low concentration (0.22 nM) improves myocardial function (systolic tension) in ischemia/reperfusion through a receptor-mediated mechanism involving release of bradykinin and prostaglandins.

Slaughterhouse blood as a perfusate for studying myocardial function under ischemic conditions

Metabolic studies using the in vitro non-recirculating blood-perfused isolated heart model require large volumes of blood. The present study was designed to determine whether heterologous pig blood collected from a slaughterhouse can be used as perfusate for isolated pig hearts perfused under aerobic and constant reduced flow conditions. Eight isolated working pig hearts perfused for 90 min at a constant flow of 1.5 ml g-1 min-1 with non-recirculated blood diluted with Krebs-Henseleit bicarbonate buffer at a hematocrit of 23% were compared to eight hearts subjected to the same protocol but perfused only with Krebs-Henseleit bicarbonate buffer solution. Hearts were paced at 100 bpm and subjected to aerobic perfusion at 38ºC. Hearts were weighed before perfusion and at the end of the experiment and the results are reported as percent weight gain (mean ± SD). Comparisons between groups were performed by the Student t-test (P<0.05). After 90 min of perfusion with modified Krebs-Henseleit, perfused hearts presented a larger weight gain than blood-perfused hearts (39.34 ± 9.27 vs 23.13 ± 5.42%, P = 0.003). Left ventricular end-diastolic pressure was higher in the modified Krebs-Henseleit-perfused group than in the blood group (2.8 ± 0.4 vs 2.3 ± 0.3 mmHg, respectively, P = 0.01). We conclude that heterologous blood perfusion, by preserving a more physiological myocardial water content, is a better perfusion fluid than modified Krebs-Henseleit solution for quantitative studies of myocardial metabolism and heart function under ischemic conditions.

Expression of inducible nitric oxide synthase is increased in patients with heart failure due to ischemic disease

The objective of the present study was to determine the relationship between nitric oxide synthases (NOS) and heart failure in cardiac tissue from patients with and without cardiac decompensation. Right atrial tissue was excised from patients with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) <35% (N = 10), and from patients with CAD and LVEF >60% (N = 10) during cardiac surgery. NOS activity was measured by the conversion of L-[H³]-arginine to L-[H³]-citrulline. Gene expression was quantified by the competitive reverse transcription-polymerase chain reaction. Both endothelial NOS (eNOS) activity and expression were significantly reduced in failing hearts compared to non-failing hearts: 0.36 ± 0.18 vs 1.51 ± 0.31 pmol mg-1 min-1 (P < 0.0001) and 0.37 ± 0.08 vs 0.78 ± 0.09 relative cDNA absorbance at 320 nm (P < 0.0001), respectively. In contrast, inducible NOS (iNOS) activity and expression were significantly higher in failing hearts than in non-failing hearts: 4.00 ± 0.90 vs 1.54 ± 0.65 pmol mg-1 min-1 (P < 0.0001) and 2.19 ± 0.27 vs 1.43 ± 0.13 cDNA absorbance at 320 nm (P < 0.0001), respectively. We conclude that heart failure down-regulates both eNOS activity and expression in cardiac tissue from patients with LVEF <35%. In contrast, iNOS activity and expression are increased in failing hearts and may represent an alternative mechanism for nitric oxide production in heart failure due to ischemic disease.

An acid-sensing ion channel that detects ischemic pain

Ischemic pain occurs when there is insufficient blood flow for the metabolic needs of an organ. The pain of a heart attack is the prototypical example. Multiple compounds released from ischemic muscle likely contribute to this pain by acting on sensory neurons that innervate muscle. One such compound is lactic acid. Here, we show that ASIC3 (acid-sensing ion channel #3) has the appropriate expression pattern and physical properties to be the detector of this lactic acid. In rats, it is expressed only in sensory neurons and then only on a minority (~40%) of these. Nevertheless, it is expressed at extremely high levels on virtually all dorsal root ganglion sensory neurons that innervate the heart. It is extraordinarily sensitive to protons (Hill slope 4, half-activating pH 6.7), allowing it to readily respond to the small changes in extracellular pH (from 7.4 to 7.0) that occur during muscle ischemia. Moreover, both extracellular lactate and extracellular ATP increase the sensitivity of ASIC3 to protons. This final property makes ASIC3 a "coincidence detector" of three molecules that appear during ischemia, thereby allowing it to better detect acidosis caused by ischemia than other forms of systemic acidosis such as hypercapnia.

Hind limb ischemic preconditioning induces an anti-inflammatory response by remote organs in rats

Ischemic preconditioning (IPC), a strategy used to attenuate ischemia-reperfusion injury, consists of brief ischemic periods, each followed by reperfusion, prior to a sustained ischemic insult. The purpose of the present study was to evaluate the local and systemic anti-inflammatory effects of hind limb IPC in male Wistar rat (200-250 g) models of acute inflammation. IPC was induced with right hind limb ischemia for 10 min by placing an elastic rubber band tourniquet on the proximal part of the limb followed by 30 min of reperfusion. Groups (N = 6-8) were submitted to right or left paw edema (PE) with carrageenan (100 µg) or Dextran (200 µg), hemorrhagic cystitis with ifosfamide (200 mg/kg, ip) or gastric injury (GI) with indomethacin (20 mg/kg, vo). Controls received similar treatments, without IPC (Sham-IPC). PE is reported as variation of paw volume (mL), vesical edema (VE) as vesical wet weight (mg), vascular permeability (VP) with Evans blue extravasation (µg), GI with the gastric lesion index (GLI; total length of all erosions, mm), and neutrophil migration (NM) from myeloperoxidase activity. The statistical significance (P < 0.05) was determined by ANOVA, followed by the Tukey test. Carrageenan or Dextran-induced PE and VP in either paw were reduced by IPC (42-58.7%). IPC inhibited VE (38.8%) and VP (54%) in ifosfamide-induced hemorrhagic cystitis. GI and NM induced by indomethacin were inhibited by IPC (GLI: 90.3%; NM: 64%). This study shows for the first time that IPC produces local and systemic anti-inflammatory effects in models of acute inflammation other than ischemia-reperfusion injury.

Texture analysis of computed tomography images of acute ischemic stroke patients

Computed tomography (CT) images are routinely used to assess ischemic brain stroke in the acute phase. They can provide important clues about whether to treat the patient by thrombolysis with tissue plasminogen activator. However, in the acute phase, the lesions may be difficult to detect in the images using standard visual analysis. The objective of the present study was to determine if texture analysis techniques applied to CT images of stroke patients could differentiate between normal tissue and affected areas that usually go unperceived under visual analysis. We performed a pilot study in which texture analysis, based on the gray level co-occurrence matrix, was applied to the CT brain images of 5 patients and of 5 control subjects and the results were compared by discriminant analysis. Thirteen regions of interest, regarding areas that may be potentially affected by ischemic stroke, were selected for calculation of texture parameters. All regions of interest for all subjects were classified as lesional or non-lesional tissue by an expert neuroradiologist. Visual assessment of the discriminant analysis graphs showed differences in the values of texture parameters between patients and controls, and also between texture parameters for lesional and non-lesional tissue of the patients. This suggests that texture analysis can indeed be a useful tool to help neurologists in the early assessment of ischemic stroke and quantification of the extent of the affected areas.

Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post-ischemic heart failure

After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1β (3.8X) and TNF-α (6.0X). IFN-γ was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.