Left Ventricle Chamber Research Articles

The Importance of Age, Sex, and Body Surface Area in Cardiovascular Dimensions Analysis

AJR 2011; 197:W966 0361–803X/11/1975–W966 © American Roentgen Ray Society The Importance of Age, Sex, and Body Surface Area in Cardiovascular Dimensions Analysis We have read with great interest the article by Nevsky and colleagues [1], which aimed to establish sex-specific normalized reference values for cardiac chamber size, wall thickness, ejection fraction, and wall and great vessels dimensions on retrospective ECG-gated cardiac CT angiography (CTA) in a population without coronary artery disease, diabetes, or arterial hypertension. The authors addressed the importance of sex-related analysis in cardiovascular dimensions, showing a significant difference in body surface area (BSA) normalized values only in left atrium and ventricle chamber size, midascending aorta, and left pulmonary artery. Several articles have previously investigated the BSA, age, and sex normalized cardiac [2, 3] and aortic [4] reference values, stressing the importance of correlating cardiovascular dimensions not only with BSA or sex but also with patient age. The age-related analysis is particularly important because the normal values in a 70-year-old patient could be pathologic in a 20-year-old patient who presented with the same sex and BSA. For this reason, a cardiovascular study should not be performed, in our opinion, without considering the patient’s age, and a complete report should include BSA, age, and sex normalized values. We conclude that the study by Nevsky et al. [1] represents an important step in this direction, and further normalization of dimensions with patient age would be helpful for defining standardized values in cardiovascular gated CTA. Carlo Nicola De Cecco Giuseppe Muscogiuri University of Rome “Sapienza,” St. Andrea Hospital, Rome, Italy Amedeo Anselmi Catholic University, Rome, Italy DOI:10.2214/AJR.11.6945 WEB—This is a Web exclusive article.

Emotional stress as a trigger of myasthenic crisis and concomitant takotsubo cardiomyopathy: a case report

IntroductionMyasthenia gravis is a neuromuscular junction post-synaptic autoimmune disorder. Myasthenic crisis is characterized by respiratory failure requiring mechanical ventilation. Takotsubo cardiomyopathy is a rare clinical syndrome defined as a profound but reversible left ventricular dysfunction in the absence of coronary artery disease.Case presentationWe report a unique case of a 60-year-old Hispanic woman with myasthenia gravis who developed takotsubo cardiomyopathy and concomitant myasthenic crisis that appear to have been triggered by a stressful life event. On admission, she presented with severe mid-sternal chest pain and shortness of breath shortly after a personally significant stressful life event. A pertinent neurological examination showed bilateral facial weakness and right ptosis. The left ventriculogram showed apical ballooning with hyperdynamic proximal segments with sparing of the apex. Her troponin I level was elevated, while cardiac catheterization revealed no significant coronary artery disease. The findings were consistent with takotsubo cardiomyopathy. Shortly after cardiac catheterization, she developed bilateral ophthalmoparesis and significant bulbar and respiratory muscle weakness. Forced vital capacity values were persistently less than 1 L. The patient developed respiratory failure and required endotracheal intubation. After plasmapheresis and corticosteroid treatment, her clinical course improved with successful extubation. A normal left ventricle chamber size and a normal ejection fraction were noted by an echocardiogram repeated 10 months later.ConclusionThis is the first reported case of the simultaneous triggering of both takotsubo cardiomyopathy and myasthenic crisis by the physiologic consequences of a state of severe emotional stress. We hypothesize that the mechanism underlying the rare association of takotsubo cardiomyopathy with myasthenic crisis involves excessive endogenous glucocorticoid release, a high-catecholamine state, or a combination of both. We advocate careful cardiac monitoring of myasthenia gravis patients during acute emotional or physical stress, as there is potential risk of developing takotsubo cardiomyopathy.

Loss of stearoyl-CoA desaturase 1 rescues cardiac function in obese leptin-deficient mice

The heart of leptin-deficient ob/ob mice is characterized by pathologic left ventricular hypertrophy along with elevated triglyceride (TG) content, increased stearoyl-CoA desaturase (SCD) activity, and increased myocyte apoptosis. In the present study, using an ob/ob;SCD1(-/-) mouse model, we tested the hypothesis that lack of SCD1 could improve steatosis and left ventricle (LV) function in leptin deficiency. We show that disruption of the SCD1 gene improves cardiac function in ob/ob mice by correcting systolic and diastolic dysfunction without affecting levels of plasma TG and FFA. The improvement is associated with reduced expression of genes involved in FA transport and lipid synthesis in the heart, as well as reduction in cardiac FFA, diacylglycerol, TG, and ceramide levels. The rate of FA beta-oxidation is also significantly lower in the heart of ob/ob;SCD1(-/-) mice compared with ob/ob controls. Moreover, SCD1 deficiency reduces cardiac apoptosis in ob/ob mice due to increased expression of antiapoptotic factor Bcl-2 and inhibition of inducible nitric oxide synthase and caspase-3 activities. Reduction in myocardial lipid accumulation and inhibition of apoptosis appear to be one of the main mechanisms responsible for improved LV function in ob/ob mice caused by SCD1 deficiency.

Effects of adiponectin deficiency on structural and metabolic remodeling in mice subjected to pressure overload

Recent data suggest adiponectin, an adipocyte-derived hormone, affects development of heart failure in response to hypertension. Severe short-term pressure overload [1-3 wk of transverse aortic constriction (TAC)] in adiponectin(-/-) mice causes greater left ventricle (LV) hypertrophy than in wild-type (WT) mice, but conflicting results are reported regarding LV remodeling, with either increased or decreased LV end diastolic volume compared with WT mice. Here we assessed the effects of prolonged TAC on LV hypertrophy and remodeling. WT and adiponectin(-/-) mice were subjected to TAC and maintained for 6 wk. Regardless of strain, TAC induced similar LV hypertrophy ( approximately 70%) and upregulation of mRNA for heart failure marker genes. However, LV chamber size was dramatically different, with classic LV dilation in WT TAC mice but concentric LV hypertrophy in adiponectin(-/-) mice. LV end diastolic and systolic volumes were lower and ejection fraction higher in adiponectin(-/-) TAC mice compared with WT, indicating that adiponectin deletion prevented LV remodeling and deterioration in systolic function. The activities of marker enzymes of mitochondrial oxidative capacity were reduced in WT TAC mice by approximately 35%, whereas enzyme activities were maintained at sham levels in adiponectin(-/-) TAC mice. In conclusion, in WT mice, long-term pressure overload caused dilated LV hypertrophy accompanied by decreased activity of mitochondrial oxidative enzymes. Although adiponectin deletion did not affect LV hypertrophy, it prevented LV chamber remodeling and preserved mitochondrial oxidative capacity, suggesting that adiponectin plays a permissive role in mediating changes in cardiac structure and metabolism in response to pressure overload.

Treatment of Heart Failure by a Methanocarba Derivative of Adenosine Monophosphate: Implication for a Role of Cardiac Purinergic P2X Receptors

Evidence is accumulating to support a potentially important role for purinergic (P2X) receptors in heart failure (HF). We tested the hypothesis that a hydrolysis-resistant nucleotide analog with agonist activity at myocardial P2X receptors (P2XRs) improves the systolic HF phenotype in mouse and dog models. We developed a hydrolysis-resistant adenosine monophosphate derivative, (1'S,2R,3S,4'R,5'S)-4-(6-amino-2-chloro-9H-purin-9-yl)-1-[phosphoryloxymethyl] bicycle[3.1.0]hexane-2,3-diol) (MRS2339), with agonist activity at native cardiac P2XRs. Chronic MRS2339 infusion in postinfarct and calsequestrin (CSQ) mice with HF resulted in higher rates of pressure change (+dP/dt), left ventricle (LV)-developed pressure, and cardiac output in an in vitro working heart model. Heart function in vivo, as determined by echocardiography-derived fractional shortening, was also improved in MRS2339-infused mice. The beneficial effect of MRS2339 was dose-dependent and was identical to that produced by cardiac myocyte-specific overexpression of the P2X(4) receptor. The HF improvement was associated with the preservation of LV wall thickness in both systole and diastole in postinfarct and CSQ mice. In dogs with pacing-induced HF, MRS2339 infusion reduced left ventricular end-diastolic pressure, improved arterial oxygenation, and increased +dP/dt. MRS2339 treatment also decreased LV chamber size in mice and dogs with HF. In murine and canine models of systolic HF, in vivo administration of a P2X nucleotide agonist improved contractile function and cardiac performance. These actions were associated with preserved LV wall thickness and decreased LV remodeling. The data are consistent with a role of cardiac P2XRs in mediating the beneficial effect of this agonist.

Assessment of the hemodynamics of left ventricle during the isovolumic contraction phase in normal snbjects by vector flow mapping

Objective To clarify whether the phase of left ventricle(LV)isovolumic contraction is the phase of hemodynamics stasis in normal subjects by using vector flow mapping(VFM).Methods Color Doppler flow images were recorded from LV apical long-axis view in fifty healthy volunteers.The characteristics of LV intracavitary flow dynamics during isovolumic contraction were analyzed by VFM.Results A global vortex occurred in the LV chamber during the late diastole which was sustained during the whole phase of isovolumic contraction.The vortex disappeared quickly in the early and middle ejection phase.The flow in the LV was initially directed toward the apex and then briefly reversed toward the base.Conclusions Isovolumic contraction phase is not the period of hemodynamic stasis but,rather,phase with dynamic changes in intracavitary flow.The vortex during isovolumic contraction makes a dynamic contribution to flow redirection and provides efficiency for momentum transfer. Key words: Echocardiography; Ventricular function,left; Hemodynamic phemomena; Vector flow mapping

Echocardiographic Evaluation of Diastolic Function Can Be Used to Guide Clinical Care

For normal cardiac performance, the left ventricle (LV) must be able to eject an adequate stroke volume at arterial pressure (systolic function) and fill without requiring an elevated left atrial (LA) pressure (diastolic function). These systolic and diastolic functions must be adequate to meet the needs of the body both at rest and during stress. Response by Tschope and Paulus on p 809 Systolic function is conveniently (although not always accurately) measured as the ejection fraction (EF), calculated as stroke volume divided by end-diastolic volume.1 The LV EF is easily interpreted. The lower limit of normal is ≈50%. The lower the EF is, the greater the reduction in systolic function. Diastolic function has been more difficult to evaluate.2 Traditionally, invasive measures of LV diastolic pressure-volume relations and the rate of LV pressure fall during isovolumetric relaxation have been used. However, these methods are not practical for routine clinical use and do not adequately evaluate all aspects of diastolic filling.3 Comprehensive echocardiographic evaluation of the dynamics of LV filling using blood pool and tissue Doppler has now progressed so that it provides clinically important information that can be used to direct patient care. We present data that support the use of echocardiographic evaluation of diastolic function to recognize cardiac dysfunction in patients with heart failure, especially those with preserved EF; to guide the management of patients by identifying those with and without elevated left filling pressures regardless of underlying EF; and to determine prognosis in a wide variety of patient populations. Although the LV end-diastolic pressure-volume relation describes the passive properties of the LV, LV filling is not a passive or slow process.3 In fact, the peak flow rate across the mitral valve is equal to or greater than the peak flow rate across the aortic valve. …

MECHANISM OF LEFT VENTRICULAR PRESSURE INCREASE DURING ISOVOLUMIC CONTRACTION, AND DETERMINATION OF ITS EQUIVALENT MYOCARDIAL FIBERS ORIENTATION

The left ventricle (LV) is modelled as a fluid-filled, thick-walled finite-elasticity cylindrical shell, subject to internal pressure increase during isovolumic contraction. Our objective is to elucidate that the tremendous internal pressure build-up during isovolumic contraction is caused by stress development in the spirally-wound myocardial fibers due to their contraction. The LV model data consists of LV chamber pressure, LV dynamic geometry and LV twist angle. In our analysis, the LV chamber pressure increase and LV (radial, longitudinal, and twist) deformations are formatted to be caused by the contractile stresses in the LV myocardial fibers (based on the hyper-elastic constitutive property of the LV myocardial wall, expressed in terms of the strain energy density function). The LV wall stresses are expressed in terms of the strain energy density function, and hence in terms of the measured LV wall strains and the material parameters. Then, by satisfying the stress boundary conditions, from the measured data on LV deformation state and LV pressure, we first determine the LV wall's constitutive properties, and then the instantaneous stress state in the LV. The stress generated in the LV cylindrical model is equivalent to the development of active compression force and torsion within the model, as a mechanism for the high intra-LV cavity pressure build-up during isovolumic contraction. We in turn adopt (i) the principal compressive stress to be the stresses developed in the myocardial fibers (by their contraction), and (ii) the principal stress trajectory to correspond to the orientation of the myocardial fibers. The results show that the myocardial fiber orientation changes during the isovolumic phase, as the LV contracts. Hence, an important determinant of our analysis is the orientation of the myocardial fibers. Conversely, it can be said that the fibers are so optimally oriented, that their contraction causes LV deformation to in turn cause the appropriate increase in intra-LV pressure. Another important outcome of our analysis is the determination of the "LV torque vs twist angle" relationship, which has the potential to be employed as an index of contractility.

J007 Cardiac remodeling following chronic activation of the Notch signaling pathway

The Notch signaling pathway is a communication system between adjacent cells, mediated by transmembrane receptors (Notch1-4) and ligands (Jagged1 and 2, Delta-like1, 3, and 4). Notch is essential for the development and homeostasis of several self-renewing organ systems. Notch is also essential in the developing heart, and mutations in Notch genes cause cardiac malformations and congenital heart disease. Recently, using loss-of-function studies, we showed that the Notch1 receptor controlled the response to injury in the adult heart by limiting myocyte hypertrophy, enhancing myocyte survival, promoting precursor proliferation, controlling cardiogenic differentiation, and reducing interstitial fibrosis. In addition, our data suggested that upregulation of Jagged1 expression constituted a primary response in the stressed myocardium, suggesting that this ligand mediated Notch signaling in the postnatal heart. Therefore, to analyze the effects of a chronic Jagged1-induced Notch activation on the cardiac response to stress, we generated transgenic mice overexpressing Jagged1 in cardiomyocytes using the α-myosin heavy chain gene promoter (TGMHCJ1 mice). These mice expressed 100-500 fold Jagged1 mRNA relative to wild-type (WT) controls. The overexpression of Jagged1 on the surface of cardiomyocytes was confirmed by Western blotting and immunofluorescence staining. Consequently, the percentage of cardiac cells with an activated Notch pathway was higher in TGMHCJ1 mice than in WT animals. The expression of the Notch target genes Hes1 and Hey2 was also activated. Echocardiographic analysis under basal conditions revealed an enlargement of the right ventricle (RV) with a diminished left ventricle (LV) mass and chamber size in adults. TGMHCJ1 mice displayed increased juvenile mortality. The severity of the phenotype was dependent on the level of Jagged1 expression. Immunofluorescence analysis revealed myocyte hypertrophy and disarray in the RV of TGMHCJ1 mice whereas, myocytes in the LV were not affected. Moreover, when subjected to transaortic constriction (TAC), TGMHCJ1 mice demonstrated an impaired LV hypertrophic response to pressure overload and reduced cardiac fibrosis. These results indicate that chronic activation of Notch affects differently left and right ventricle integrity under physiological and pathological conditions.

Fish oil, but not flaxseed oil, decreases inflammation and prevents pressure overload-induced cardiac dysfunction

Clinical studies suggest that intake of omega-3 polyunsaturated fatty acids (omega-3 PUFA) may lower the incidence of heart failure. Dietary supplementation with omega-3 PUFA exerts metabolic and anti-inflammatory effects that could prevent left ventricle (LV) pathology; however, it is unclear whether these effects occur at clinically relevant doses and whether there are differences between omega-3 PUFA from fish [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] and vegetable sources [alpha-linolenic acid (ALA)]. We assessed the development of LV remodelling and pathology in rats subjected to aortic banding treated with omega-3 PUFA over a dose range that spanned the intake of humans taking omega-3 PUFA supplements. Rats were fed a standard food or diets supplemented with EPA+DHA or ALA at 0.7, 2.3, or 7% of energy intake. Without supplementation, aortic banding increased LV mass and end-systolic and -diastolic volumes. ALA supplementation had little effect on LV remodelling and dysfunction. In contrast, EPA+DHA dose-dependently increased EPA and DHA, decreased arachidonic acid in cardiac membrane phospholipids, and prevented the increase in LV end-diastolic and -systolic volumes. EPA+DHA resulted in a dose-dependent increase in the anti-inflammatory adipokine adiponectin, and there was a strong correlation between the prevention of LV chamber enlargement and plasma levels of adiponectin (r = -0.78). Supplementation with EPA+DHA had anti-aggregatory and anti-inflammatory effects as evidenced by decreases in urinary thromboxane B(2) and serum tumour necrosis factor-alpha. Dietary supplementation with omega-3 PUFA derived from fish, but not from vegetable sources, increased plasma adiponectin, suppressed inflammation, and prevented cardiac remodelling and dysfunction under pressure overload conditions.

Cardiovascular response to acute hypoxemia induced by prolonged breath holding in air

Prolonged breath hold (BH) represents a valid model for studying the cardiac adaptation to acute hypoxemia in humans. Cardiac magnetic resonance (CMR) allows a three-dimensional, high-resolution, noninvasive, and nonionizing anatomical and functional evaluation of the heart. The aim of the study was to assess the adaptation of the cardiovascular system to prolonged BH in air. Ten male volunteer diving athletes (age 30 +/- 6 yr) were studied during maximal BH duration with CMR. Four epochs were studied: I, rest; II and III, intermediate BH; and IV, peak BH. Oxygen saturation (So(2)), heart rate (HR), blood pressure (BP), systemic vascular resistance (VR), end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), ejection fraction (EF), maximal elastance index (EL), systolic wall thickening (SWT), and end-systolic wall stress (ESWS) of the left ventricle (LV) were measured in all four BH epochs. Average BH duration was 3.7 +/- 0.3 min. So(2) was reduced (I: 97 +/- 0.2%, range 96-98%, vs. IV: 84 +/- 2.0%, range 76-92%; P < 0.00001). BP, EDV, ESV, SV, CO, and ESWS linearly increased from epochs I to IV, whereas EF, EL, and SWT showed an opposite behavior, decreasing from resting to epoch IV (all trends are P < 0.01). During prolonged BH in air, a marked enlargement of the LV chamber occurs in healthy diving athletes. This response to acute hypoxemia allows SV,CO, and arterial pressure to be maintained despite the severe reduction in LV contractile function.

Abstract 555: Heme-Oxygenase 1 Upregulation Attenuates Acute Myocardial Reperfusion Injury and Left Ventricular Remodeling in Rats

Background: Reperfusion injury occurring after reestablishment of blood flow after MI is thought to be mediated by reactive oxygen species and neutrophilic cellular damage. The Heme-Oxygenase-1 (HO-1) dependent decrease in oxidative stress may attenuate injury in part by inhibiting transcription factor NFκB-mediated inflammation. We tested the hypothesis that exogenous upregulation of HO-1 by hemin administration confers acute and chronic cardioprotection against I/R injury in rats and attenuates LV remodeling post-infarction. Methods: Six week-old male Wistar rats were randomly assigned to sham, vehicle, or hemin-treated groups. Vehicle and hemin were administered i.p. once daily for 3 days prior to LAD occlusion, and 48 hours post-operatively once every 3 days. Infarct size was determined by H&amp;E histological analysis and fibrosis was quantified by Masson’s Trichrome staining. We used transthoracic echocardiography to assess LV size, function and wall motion. Results: Hemin increased HO-1 expression and decreased infarct size and fibrosis, and attenuated LV wall thinning and chamber dilatation in the short-term (4 days post-infarction). The decrease in infarct size and fibrosis in the hemin group was accompanied by a decrease in NF-κB activity. We observed no significant difference in infarct size and area of fibrosis between hemin and vehicle-treated groups at 3 months (p=0.6681, p=0.6382, respectively). Cavity dilatation did not differ between the two groups at 3 months, however attenuated interventricular septum thinning (p&lt;0.05) was observed in the hemin group compared with the vehicle group. Conclusion: HO-1 upregulation by hemin confers acute cardioprotection and decreased inflammation, possibly by inhibiting NF-κB activity, although chronic treatment with hemin does not prevent long-term LV remodeling post-MI. Future research should focus on optimal HO-1 upregulation to attenuate long-term LV remodeling due to reperfusion injury. Left Ventricle Wall and Chamber Dimensions

Tako‐Tsubo cardiomyopathy

Tako-Tsubo cardiomyopathy is characterized by a typically transient hypo-to-akinesis with ballooning of the apical portion of the left ventricle (LV) in the absence of major vascular impairment 1. Compensatory hyperkinetic wall motion of the basal portion of the LV chamber has been described in a recent issue of this Journal 2. Although emotional or physical stresses are commonly invoked as possible triggers in a majority of reported cases, the pathophysiology of the underlying mechanisms has remained largely elusive. Sudden systemic sympathetic activation with transiently excessive levels of plasma catecholamines, causing either metabolic or microvascular impairment in the LV apical zone, has been suggested 3. Regional dysfunction of right ventricular (RV) wall motion may also be involved 4. In the absence of any definitive explanation, we would like to call attention to the additional possibility that a transient dysfunction of the endocardial endothelium lining the apical, highly trabeculated LV myocardium could also be a plausible cause of a reversible dysfunction of the apical LV myocardium. Previous work has shown that endocardial and capillary endothelial-to-myocardial interactions are obligatory for normal cardiac function 5,6. Interaction of the endocardial endothelium with circulating substances and constituents in the blood may thereby modulate subjacent myocardial performance 789. The transmural inner cavitary half of the apical portion of the LV wall is highly trabeculated; in fact, the apical LV myocardium is the thinnest and most densely trabeculated — or, most non-compaction — myocardium of the LV. The more trabeculated the myocardium in any given portion of the ventricular wall, the higher the surface-to-volume ratio, and hence the more exposed the endocardial endothelial surface lining that area. Accordingly, along with the intensively trabeculated RV surface, the apical trabeculated LV wall may become a most vulnerable target when exposed to excessive plasma levels of substances, like catecholamines, known to affect or damage the endocardial endothelial cells 7,10. In Tako-Tsubo cardiomyopathy, catecholamine-induced endocardial endothelial dysfunction could, therefore, be expected to preferentially affect these LV areas with the highest surface-to-volume ratio, and hence contribute to a transient impairment of the contractile performance of the subjacent, apical LV myocardium, as well as of some zones in the RV. Although this conjecture can presently hardly be proven experimentally, as there are as yet no in vivo markers of endocardial endothelial (dys)function available, we suggest to nevertheless add it to the already exhaustive list of putative mechanisms.

3D Echocardiography: A Review of the Current Status and Future Directions

Ultrasound technology has improved markedly in the past 10 to 15 years, prompting echocardiographers to extend its use in studying cardiac structure and function. New ultrasound equipment and techniques offer superior image quality, greater accuracy, and expanding capabilities. As a result, more and improved imaging modalities are available for evaluating cardiac anatomy, ventricular function, blood flow velocity, and valvular diseases. Threedimensional (3D) echocardiography offers the ability to improve and expand the diagnostic capabilities of cardiac ultrasound. However, as with any emerging technology, the enthusiasm to embrace a new technique must be tempered by a critical appraisal of the evidence supporting its use. It is essential to assess the limitations as well as the unique capabilities it provides. Cardiac imaging should be safe, accurate, versatile, comprehensive, and cost-effective, while providing important clinical information. Criteria for appropriate utilization should be based on current evidence and updated as new information becomes available. To justify the use of a new 3D modality, its unique contribution to clinical practice must be critically analyzed. In this article we review the status of 3D echocardiography, examine the evidence for its use in various clinical situations, and propose guidelines for appropriate application of this technique based on available evidence.

The effect of a myocardial infarction on the normalized time-varying elastance curve

It has been suggested that the shape of the normalized time-varying elastance curve [E(n)(t(n))] is conserved in different cardiac pathologies. We hypothesize, however, that the E(n)(t(n)) differs quantitatively after myocardial infarction (MI). Sprague-Dawley rats (n = 9) were anesthetized, and the left anterior descending coronary artery was ligated to provoke the MI. A sham-operated control group (CTRL) (n = 10) was treated without the MI. Two months later, a conductance catheter was inserted into the left ventricle (LV). The LV pressure and volume were measured and the E(n)(t(n)) derived. Slopes of E(n)(t(n)) during the preejection period (alpha(PEP)), ejection period (alpha(EP)), and their ratio (beta = alpha(EP)/alpha(PEP)) were calculated, together with the characteristic decay time during isovolumic relaxation (tau) and the normalized elastance at end diastole (E(min)(n)). MI provoked significant LV chamber dilatation, thus a loss in cardiac output (-33%), ejection fraction (-40%), and stroke volume (-30%) (P < 0.05). Also, it caused significant calcium increase (17-fold), fibrosis (2-fold), and LV hypertrophy. End-systolic elastance dropped from 0.66 +/- 0.31 mmHg/microl (CTRL) to 0.34 +/- 0.11 mmHg/microl (MI) (P < 0.05). Normalized elastance was significantly reduced in the MI group during the preejection, ejection, and diastolic periods (P < 0.05). The slope of E(n)(t(n)) during the alpha(PEP) and beta were significantly altered after MI (P < 0.05). Furthermore, tau and end-diastolic E(min)(n) were both significantly augmented in the MI group. We conclude that the E(n)(t(n)) differs quantitatively in all phases of the heart cycle, between normal and hearts post-MI. This should be considered when utilizing the single-beat concept.

Direct Left Ventricle-to-Coronary Artery Stent Restores Perfusion to Chronic Ischemic Swine Myocardium

Direct left ventricle (LV)-to-coronary artery shunts (VSTENT) have been proposed as an alternative means of myocardial revascularization. The goal of this study was to examine quantitative changes in myocardial perfusion and possible mechanisms of revascularization with an LV-to-coronary shunt. Ameroid occluders were implanted on the proximal left anterior descending coronary artery (LAD) of 6 pigs to create chronic ischemia. Four weeks later, a VSTENT was placed to directly connect the distal LAD with the LV chamber. Animals survived for an additional 3 weeks and received periodic bromodeoxyuridine (BrdU) injections to identify dividing cells to identify and quantify angiogenesis. Regional myocardial perfusion (RMP) was measured with color microspheres under adenosine vasodilatory stress before and 3 weeks after VSTENT implantation. Vascularity was assessed histologically by an overall vascularity index and a growth index reflecting the density of BrdU-positive vascular cells. Three weeks after VSTENT placement, RMP improved from 38.4% +/- 19.6% of non-ischemic flow to 86.8% +/- 13.7% in treated animals (P < .05). This benefit was accompanied by histological evidence of increased vascularity and vascular proliferation. Four of 5 animals had patent and functional devices at the end of the study. Chronic VSTENT placement improves RMP and may promote arterial remodeling in chronically ischemic porcine myocardium.

Takotsubo Cardiomyopathy after General Anesthesia for Eye Surgery

Takotsubo Cardiomyopathy after General Anesthesia for Eye Surgery

Heme oxygenase‐1 (HO‐1) inhibits postmyocardial infarct remodeling and restores ventricular function

We reported previously that predelivery of the anti-oxidant gene heme oxygenase-1 (HO-1) to the heart by adeno associated virus (AAV) markedly reduces injury after acute myocardial infarction (MI). However, the effect of HO-1 gene delivery on postinfarction recovery has not been investigated. In the current study, we assessed the effect of HO-1 gene delivery on post-MI left ventricle (LV) remodeling and function using echocardiographic imaging and histomorphometric approaches. Two groups of Sprague-Dawley rats were injected with 4 x 10(11) particles of AAV-LacZ (control) or AAV-hHO-1 in the LV wall. Eight wk after gene transfer, the animals were subjected to 30 min of ischemia by ligation of left anterior descending artery (LAD) followed by reperfusion. Echocardiographic measurements were obtained in a blinded fashion prior and at 1.5 and 3 months after I/R. Ejection fraction (EF) was reduced by 13% and 40% in the HO-1 and LacZ groups, respectively at 1.5 months after MI. Three months after MI, EF recovered fully in the HO-1, but only partially in the LacZ-treated animals. Post-MI LV dimensions were markedly increased and the anterior wall was markedly thinned in the LacZ-treated animals compared with the HO-1-treated animals. Significant myocardial scarring and fibrosis were observed in the LacZ-group in association with elevated levels of interstitial collagen I and III and MMP-2 activity. Post-MI myofibroblast accumulation was reduced in the HO-1-treated animals, and retroviral overexpression of HO-1 reduced proliferation of isolated cardiac fibroblasts. Our data indicate that rAAV-HO-1 gene transfer markedly reduces fibrosis and ventricular remodeling and restores LV function and chamber dimensions after myocardial infarction.

Physiologic Compensation Is Supranormal in Compensated Aortic Stenosis: Does it Return to Normal After Aortic Valve Replacement or Is it Blunted by Coexistent Coronary Artery Disease?

In compensated aortic stenosis (AS), cardiac performance measured at the ventricular chamber is typically supranormal, whereas measurements at the myocardium are often impaired. We investigated intramyocardial mechanics after aortic valve replacement (AVR) and the effects relative to the presence or absence of coronary artery disease (CAD+ or CAD-), respectively. Twenty-nine patients (46 to 91 years, 10 female) with late but not decompensated AS underwent cardiovascular MRI before AVR (PRE), with follow-up at 6+/-1 (EARLY) and 13+/-2 months (LATE) to determine radiofrequency tissue-tagged left ventricle (LV) transmural circumferential strain, torsion, structure, and function. At the myocardial level, concentric LV hypertrophy regressed 18% LATE (93+/-22 versus 77+/-17 g/m2; P<0.0001), whereas at the LV chamber level, ejection fraction was supranormal PRE, 67+/-6% (ranging as high as 83%) decreasing to 59+/-6% LATE (P<0.05), representing not dysfunction but a return to more normal LV physiology. Between the CAD+ and CAD- groups, intramyocardial strain was similar PRE (19+/-10 versus 20+/-10) but different LATE, with dichotomization specifically related to the CAD state. In the CAD- patients, strain increased to 23+/-10% (+20%), whereas in CAD+ patients it fell to 16+/-11% (-26%), representing a nearly 50% decline after AVR (P<0.05). This was particularly evident at the apex, where CAD- strain LATE improved 17%, whereas for CAD+ it decreased 2.5-fold. Transmural strain and myocardial torsion followed a similar pattern, critically dependent on CAD. AVR impacted LV geometry and mitral apparatus, resulting in decreased mitral regurgitation, negating the double valve consideration. In AS patients after AVR, reverse remodeling of the supranormal systolic function parallels improvement in cardiovascular MRI-derived regression of LV hypertrophy and LV intramyocardial strain. However, discordant effects are evident after AVR, driven by CAD status, suggesting that the typical AVR benefits are experienced disproportionately by those without CAD and not by those obliged to undergo concomitant coronary artery bypass grafting/AVR.

Management of pulmonary hypertension: physiological and pharmacological considerations for anesthesiologists.

For decades the pulmonary circulation was not considered as important as the systemic (“greater”) circulation. However, pulmonary hypertension can arise because of many diseases of the heart and lung. Therefore, increasing efforts in research have been undertaken leading to a profound increase in un