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  • 1
    Electronic Resource
    Electronic Resource
    Acute Ventricular Reduction with the Acorn Cardiac Support Device: Effect on Progressive Left Ventricular Dysfunction and Dilation in Dogs with Chronic Heart Failure (2001)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiac surgery 16 (2001), S. 0 
    Details
    ISSN: 1540-8191
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background and Aim: Surgical resection of myocardium that acutely reduces left ventricular (LV) volume in patients with advanced heart failure (HF), the so-called “Batista Operation,” remains controversial. We examined the effects of acute LV reduction with the Acorn Cardiac Support Device (CSD) in dogs with HF (LV ejection fraction 〈 30%). Methods: HF was produced in 15 dogs by intracoronary microembolization. In nine dogs, intravenous dobutamine was administered to reduce LV end-diastolic dimension (LVEDD) by 10%-25%. While on dobutamine infusion, the CSD, a preformed knitted polyester device, was surgically placed around the ventricles, anchored to the arteriovenous (AV) groove, and tailored anteriorly to fit snugly over the ventricles. Dogs were then weaned off dobutamine. Results: On average, the procedure reduced LVEDD by 7 ± 1 mm (range 5–12 mm). Of the nine dogs, two died before completion of the study and seven survived for the entire period. Six dogs did not undergo device placement and served as controls. All were followed for 3 months prior to sacrifice. In controls, LV end-diastolic volume increased after 3 months (66 ± 5 mL vs 77 ± 6 mL; p = 0.007), while in CSD-treated dogs (n = 7), it decreased (80 ± 5 mL vs 60 ± 3 mL; p = 0.002). In controls, LV ejection fraction (EF) decreased after 3 months (27 ± 1% vs 23 ± 1%; p = 0.001) but was unchanged in CSD-treated dogs (25 ± 1% vs 26 ± 1%; p = 0.66). Compared to controls, CSD-treated dogs showed improved LV diastolic dysfunction and chamber sphericity, decreased wall stress, and no functional mitral regurgitation (MR). Conclusion: In dogs with advanced HF, acute LV reduction with the Acorn CSD prevents progressive global LV dilatation and ameliorates functional MR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8191.2001.tb00496.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mechanical Factors in the Degeneration of Porcine Bioprosthetic Valves: An Overview (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiac surgery 4 (1989), S. 0 
    Details
    ISSN: 1540-8191
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Predilection of certain sites of the porcine bioprosthetic valve (PBV) leaflets to calcification and tissue disruption has provoked suggestions that design factors and mechanical stresses may be major reasons leading to degeneration. In recent years, computer based numerical models of PBVs have shown a close association between sites of leaflet calcification and disruption and sites of leaflet stress concentration. These numerical models have also provided a means through which methodical design optimization can be carried out. Increasing stent flexibility, for instance, was shown to lead to an overall reduction of mechanical stresses on the PBV leaflets. Reducing the stent height, on the other hand, was accompanied by an undesirable increase of overall leaflet stresses. Despite encouraging work in this field, more research is needed to further elucidate means by which the structural integrity of bioprosthetic valves can be preserved through a minimization of the adverse effects of mechanical stresses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1540-8191.1989.tb00294.x
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  • 3
    Electronic Resource
    Electronic Resource
    RELATION OF INTRAMYOCARDIAL PRESSURE TO CORONARY PRESSURE AT ZERO FLOW (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 13 (1986), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The purpose of this study was to determine the extent to which coronary pressure at zero coronary flow (Pf=0) may relate to extravascular compressive forces determined by direct measurements of left ventricular intramyocardial pressure.2. Studies were performed in nine open-chest anaesthetized dogs in which the anterior descending coronary artery was cannulated and perfused from the carotid artery. Coronary pressure was measured at the tip of the cannula.3. Intramyocardial pressure was measured with a 1 mm diameter micromanometer inserted directly into the subepicardium. The atrioventricular node was obliterated by cautery and the heart was electrically paced. Long diastolic pauses, sufficient to allow coronary flow to reach zero, were produced by the cessation of electrical pacing.4. In the autoregulated coronary bed, Pf=0, 47 mmHg (s.e.m. = 9), exceeded subepicardial pressure at zero flow, 23 mmHg (s.e.m. =2; P 〈 0.001). During maximal vasodilatation with adenosine, Pf=0, 16 mmHg (s.e.m. = 11), was not significantly different from subepicardial pressure at zero flow, 21 mmHg (s.e.m. =4). These observations indicate that, in addition to coronary vasomotor tone, diastolic myocardial tissue pressure is important in the genesis of Pf=0.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1986.tb00928.x
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  • 4
    Electronic Resource
    Electronic Resource
    Ventricular remodeling: insights from pharmacologic interventions with angiotensin-converting enzyme inhibitors (1995)
    Springer
    Molecular and cellular biochemistry 147 (1995), S. 51-55 
    Details
    ISSN: 1573-4919
    Keywords: ventricular enlargement ; myocyte hypertrophy ; interstitial fibrosis ; angiotensin converting enzyme inhibitors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Structural remodeling of the left ventricular (LV) myocardium develops in a time-dependent fashion following acute myocardial infarction and may be an integral component in the transition toward overt heart failure. Globally, the remodeling process is characterized by progressive LV enlargement and increased chamber sphericity. At the cellular level, the remodeling process is associated with myocyte slippage, hypertrophy, and accumulation of collagen in the interstitial compartment. In the present study, we examined the effects of early, long-term monotherapy with the angiotensin converting enzyme (ACE) inhibitor, enalapril, on the progression of LV remodeling in dogs with LV dysfunction (ejection fractions 30–40%) produced by multiple sequential intracoronary microembolizations. Dogs were randomized to 3 months oral therapy with enalapril (n=7) or to no treatment (n=7). In untreated dogs, LV end-systolic volume index (ESVI), end-diastolic volume index (EDVI) and chamber sphericity increased significantly during the 3 months follow-up period. In contrast, in dogs treated with enalapril ESVI, EDVI and chamber sphericity remained essentially unchanged. Treatment with enalapril attenuated myocyte hypertrophy and the accumulation of interstitial collagen in comparison to untreated dogs. These data indicate that early treatment with ACE inhibitors can prevent the progression of LV remodeling in dogs with LV dysfunction. Afterload reduction, inhibition of direct action of angiotensin-II and possibly the decrease in bradykinin degradation elicited by ACE inhibition may act in concert in preventing the progression LV chamber remodeling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944783
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  • 5
    Electronic Resource
    Electronic Resource
    Progression of heart failure: A role for interstitial fibrosis (1995)
    Springer
    Molecular and cellular biochemistry 147 (1995), S. 29-34 
    Details
    ISSN: 1573-4919
    Keywords: heart failure ; ventricular function ; interstitial fibrosis ; coronary microcirculation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Progressive deterioration of left ventricular (LV) function is a characteristic feature of the heart failure (HF) state. The mechanism or mechanisms responsible for this hemodynamic deterioration are not known but may be related to progressive intrinsic dysfunction, degeneration and loss of viable cardiocytes. In the present study, we tested the hypothesis that accumulation of collagen in the cardiac interstitium (reactive interstitial fibrosis, RIF), known to occur in HF, results in reduced capillary density (CD=capillary/fiber ratio) and increased oxygen diffusion distance (ODD) which can lead to hypoxia and dysfunction of the collagen encircled myocyte. Studies were performed in LV tissue obtained from 10 dogs with chronic HF (LV ejection fraction 26±1%) produced by multiple sequential intracoronary, microembolizations. In each dog, CD and ODD were evaluated in LV regions that manifested severe RIF (volume fraction 16±2%) and in LV regions of little or no RIF (volume fraction 4±1%). In regions of severe RIF, CD was significantly decreased compared to regions of no RIF (0.92±0.02 vs. 1.05±0.03) (P〈0.03). Similarly, ODD was significantly increased in regions of severe RIF compared to regions of no RIF (15.3±0.4 vs. 12.2±0.3 μm) (P〈0.001). These data suggest that in dogs with chronic HF, constituent myocytes of LV regions which manifest severe RIF may be subjected to chronic hypoxia; a condition that can adversely impact the function and viability of the collagen encircled cardiocyte.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944780
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  • 6
    Electronic Resource
    Electronic Resource
    Coronary extravascular compression influences systolic coronary blood flow (1986)
    Springer
    Heart and vessels 2 (1986), S. 140-146 
    Details
    ISSN: 1615-2573
    Keywords: Coronary extravascular compression ; Systolic coronary flow ; LV subepicardial pressure ; Intracoronary isoproterenol ; Maximal vasodilation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this study was to determine whether a relation exists between systolic coronary blood flow and systolic coronary extravascular compressive forces. Studies were performed in seven open-chest dogs in which the left anterior descending coronary artery was cannulated and perfused from the left carotid artery. Pressure within the left ventricular subepicardium, a measure of coronary extravascular compression in the subepicardium, was measured with a 1-mm-diameter catheter-tip micromanometer inserted directly into the myocardium in the region of perfusion. Systolic extravascular compressive forces were augmented by a local intracoronary injection of 1µg isoproterenol. Measurements were made in the presence of coronary vasomotor tone and were repeated following local maximal vasodilatation with adenosine. In the regulated coronary bed, systolic coronary flow decreased (18±4 vs −2±4 ml/min,P〈0.01) as intramyocardial pressure increased (127±5 vs 222±12 mmHg,P〈0.001). Similarly, in the maximally vasodilated coronary bed, systolic coronary flow decreased (103±16 vs 38±11 ml/min,P〈0.001) as intramyocardial pressure increased (112±6 vs 204±16 mmHg,P〈0.001). These observations indicate that an augmentation of coronary extravascular compressive forces during systole is accompanied by a diminution of systolic coronary flow irrespective of coronary vasomotor tone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02128139
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  • 7
    Electronic Resource
    Electronic Resource
    Cardiomyocyte Apoptosis in Experimental Health Failure (1998)
    Springer
    Heart failure reviews 3 (1998), S. 35-43 
    Details
    ISSN: 1573-7322
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Heart failure is characterized by progressive worsening of left ventricular (LV) function over time. The mechanism(s) responsible for this hemodynamic deterioration are not known. It is often assumed, but by no means established, that progressive LV dysfunction results largely from ongoing loss of functional cardiac units. If ongoing myocyte loss occurs during the course of evolving heart failure and can indeed account for the progressive deterioration of LV dysfunction, then the identification of factors responsible for this loss of muscle mass can potentially lead to novel therapeutic modalities aimed at preventing the transition toward intractable heart failure. Recent studies in experimental animals have shown that cardiac myocyte loss through apoptosis, or programmed cell death, occurs 1) following myocardial infarction, 2) in the presence of cardiac hypertrophy, 3) in the aging heart, and 4) in the setting of chronic heart failure. The observation of myocyte apoptosis in experimental animal models of heart failure has since been confirmed in the failed human heart. Considerable work has also been accomplished, and credible concepts advanced, in an attempt to uncover the physiological and molecular triggers of myocyte apoptosis in heart failure. While, at present, one can comfortably accept the existence of the phenomenon of myocyte apoptosis in the failing heart, two integral questions remain essentially unanswered. First, what pathophysiological factors(s), inherent to heart failure, trigger myocyte apoptosis? Second, how important is myocyte apoptosis in the progression of LV dysfunction and the transition to overt failure? The present article will summarize our current knowledge of myocyte apoptosis based largely on data available from animal models of myocardial infarction, hypertrophy, and failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009702513648
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  • 8
    Electronic Resource
    Electronic Resource
    Hemodynamic Effects of a Novel Sodium Channel Activator in Dogs With Chronic Heart Failure (2000)
    Springer
    Cardiovascular drugs and therapy 14 (2000), S. 77-82 
    Details
    ISSN: 1573-7241
    Keywords: congestive heart failure ; sodium channel ; ventricular function ; inotropic agents ; animal models
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The use of positive inotropic agents, such as sympathomimetics and phosphodiesterase inhibitors, in heart failure (HF) is limited by proarrhythmic and positive chronotropic effects. In the present study, we compared the hemodynamic effects of intravenous LY366634 (LY), a Na+ channel enhancer, with dobutamine (DOB), in eight dogs with HF produced by intracoronary microembolizations. We also determined whether intravenous LY has synergistic effects when combined with digoxin. After baseline measurements, infusion of DOB was initiated at a dose of 2 µg/kg/min and increased until an increase of heart rate (HR) 〉30% of baseline or ventricular arrhythmias developed. Once hemodynamics returned to baseline, LY was infused at a dose of 2 µg/kg/min and increased until the LV fractional area of shortening (FAS), determined echocardiographically, reached a similar level as with DOB. Both drugs increased FAS equivalently compared to baseline (DOB, 24 ± 3 to 47 ± 2; LY, 27 ± 2 to 46 ± 2%). DOB increased HR from 78 ± 4 min-1 at baseline to 107 ± 7 min-1 at maximal dose (p 〈 0.05) and provoked serious arrhythmias in one dog. In contrast, LY infusion did not increase HR (82 ± 7 vs. 80 ± 8 min-1) or elicit arrhythmias. After 1 week of oral digoxin, dogs were infused again with LY. A lower dose of LY was needed to achieve the same increase in FAS compared to LY alone, but this was not statistically significant. The combination of LY with digoxin did not increase HR or evoke arrhythmias. We conclude that in dogs with HF, intravenous LY improves LV function to the same extent as DOB without increasing HR or evoking ventricular arrhythmias. The combination of LY with digoxin elicits a safe positive inotropic response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007899307128
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  • 9
    Electronic Resource
    Electronic Resource
    Cell Death, Tissue Hypoxia and the Progression of Heart Failure (2000)
    Springer
    Heart failure reviews 5 (2000), S. 131-138 
    Details
    ISSN: 1573-7322
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An important feature of heart failure is the progressive deterioration of left ventricular function that occurs in the absence of clinically apparent intercurrent adverse events. The mechanism or mechanisms responsible for this hemodynamic deterioration are not known. We and others have advanced the hypothesis that this hemodynamic deterioration results from progressive intrinsic contractile dysfunction of viable cardiomyocytes and/or from ongoing loss of cardiomyocytes. This review will focus on the concept of ongoing cardiac myocyte loss as a contributing factor to the progression of left ventricular dysfunction that characterizes the heart failure state. Specifically, the discussion will center on apoptosis or “programmed cell death” as a potential mediator of cardiomyocyte loss. In recent years, several studies have shown that constituent myocytes of failed explanted human hearts and hearts of animals with experimentally induced heart failure undergo apoptosis. Studies have also shown that cardiomyocyte apoptosis occurs following acute myocardial infarction, in the hypertrophied heart as well as in the aging heart; conditions frequently associated with the development of failure. While available data support the existence of myocyte apoptosis in the failing heart, lacking are studies which address the importance of myocyte apoptosis in the progression of LV dysfunction. As part of this discussion, we will address this issue and construct a case in support of a concept that the failing myocardium is subject to regional hypoxia, an abnormality that can potentially trigger cardiomyocyte apoptosis. If loss of cardiac myocytes through apoptosis can be shown to be an important contributor to the progression of heart failure, and if exact physiologic and molecular factors that trigger apoptosis in the heart can be identified, the stage will be set for the development of novel therapeutic modalities aimed at preventing, or at the very least retarding, the process of progressive ventricular dysfunction and the ultimate transition toward end-stage, intractable heart failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009880720032
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  • 10
    Electronic Resource
    Electronic Resource
    Hemodynamic response of a canine model of chronic heart failure to intravenous dobutamine, nitroprusside, enalaprilat, and digoxin (1993)
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 349-356 
    Details
    ISSN: 1573-7241
    Keywords: heart failure ; dobutamine ; nitroprusside ; enalaprilat ; digoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The hemodynamic effects of acute intravenous administration of nitroprusside, dobutamine, enalaprilat, and digoxin was investigated in a canine model of chronic heart failure (CHF) produced by multiple sequential intracoronary microembolizations. Dobutamine (4 µg/kg/min) increased cardiac output (2.4±0.1 vs. 4.0±0.4 l/min; p〈.001) and LV ejection fraction (LVEF; 26±1 vs. 30±4%; p〈.01), and decreased systemic vascular resistance (SVR; 3620±170 vs. 2470±190 dynes sec cm−5; p〈.001). Nitroprusside (3 µg/kg/min) acted as a venodilator; it decreased pulmonary artery wedge pressure (16±1 vs. 13±1 mmHg; p〈.01) and SVR (3730±440 vs. 3210±280 dynes sec cm−5; NS) but had no effect on cardiac output. Enalaprilat (1.875 mg) produced a significant increase of cardiac output (3.0±0.5 vs. 3.8±0.5 l/min; p〈.001) and LVEF (22±1 vs. 30±1%; p〈.01), and decreased SVR (3280±400 vs. 2450±250 dynes sec cm−5; p〈.01). Intravenous digoxin at a cumulative dose of 0.75 mg increased LVEF (23±2 vs. 31±2%; p〈.01) but had no effect on SVR. These data indicate that this canine model of CHF responds to acute pharmacologic intervention in a manner comparable to that seen in patients with CHF. Accordingly, this model may be a useful tool for the preclinical evaluation of new drugs targeted toward the treatment of CHF and for investigating the mechanisms of action of drugs currently used for the treatment of this disease state.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00880158
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