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  • 1
    Online Resource
    Online Resource
    Hemodynamic and Metabolic Responses to Vasodilator Therapy in Acute Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 1973
    In:  Circulation Vol. 48, No. 6 ( 1973-12), p. 1183-1193
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 48, No. 6 ( 1973-12), p. 1183-1193
    Abstract: Hemodynamic effects of vasodilator therapy (phentolamine or nitroprusside) were studied in 38 patients with acute myocardial infarction (AMI). Cardiac metabolism was studied in 19 of the 38 patients. According to the initial level of left ventricular filling pressure (LVFP) and left ventricular stroke work index (SWI), patients were divided into three groups: Group I-nine pa- tients with LVFP 15 mm Hg or less; Group II-14 patients with LVFP 〉 15 mm Hg and SWI 〉 20 g-m/m 2 ; Group III-15 patients with LVFP 〉 15 mm Hg and SWI 〈 20 g-m/ m 2 . In Group I most patients were clinically uncomplicated. In Group IL most patients had clinical left ventricular failure including one patient who had clinical features of cardiogenic shock. Group III patients all had severe left ventricular failure, with eight patients in clinical shock. In all groups LVFP, pulmonary artery pressure, right atrial pressure, and systemic and pulmonary vascular resistance decreased significantly with vasodilator therapy with only a slight to moderate decrease in arterial pressure. In Group I patients SVI decreased (-7%) together with an increase in heart rate. Significant improvement in left ventricular performance, however, was observed in Groups II and III as indicated by increased stroke volume index (SVI) and cardiac index (CI) and decreased LVFP. The increase in SVI and CI was of similar magnitude in both Group LI (SVI +18%, CI +24%) and Group III (SVI +28%, CI +29%) patients, a change suggesting that vasodilation thereby may be applicable and beneficial even in the presence of severe depression of cardiac performance. Improved left ventricular performance in group II and III patients was accompanied by a slight decrease in coronary blood flow, myocardial oxygen consumption, and transmyocardial oxygen extraction. There was no change in myocardial lactate metabolism in any group. In vitro studies in isolated cat papillary muscle preparations showed no direct positive inotropic effect of either phentolamine or nitroprusside. Thus, significant improvement in left ventricular performance occurs during vasodilator therapy in patients with AMI and elevated LVFP, even in the presence of severe depression of cardiac performance. Furthermore, this improvement is not accompanied by increased metabolic cost. Vasodilator therapy, therefore, may have an important role in the treatment of pump failure complicating myocardial infarction.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.48.6.1183
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1973
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  • 2
    Online Resource
    Online Resource
    Effects of Isometric Exercise on Cardiac Performance : The Grip Test
    Ovid Technologies (Wolters Kluwer Health) ; 1971
    In:  Circulation Vol. 44, No. 6 ( 1971-12), p. 994-1002
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. 6 ( 1971-12), p. 994-1002
    Abstract: Twenty-two patients with heart disease performed a standard isometric exercise, sustained handgrip, during the course of diagnostic cardiac catheterization. During handgrip an increase in mean arterial pressure (average 87 to 104 mm Hg) was noted in all patients. Coronary sinus blood flow and myocardial O 2 consumption increased (average 45%) in all patients so monitored. Systemic vascular resistance increased in 19 patients, in contrast to the response reported in normal volunteers. The relation between left ventricular stroke-work index and LVEDP (left ventricular function curve) during the control state and during the fourth minute of sustained handgrip provided a simple estimate of left ventricular reserve and correlated well with the New York Heart Association functional classification of the patient studied. Patients with good reserve had a rise in stroke-work with little or no change in LVEDP. Patients with poor reserve had a fall in stroke-work together with a substantial rise in LVEDP. It is concluded that the stress imposed by sustained handgrip provides a simple test for the evaluation of left ventricular reserve.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.44.6.994
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1971
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  • 3
    Online Resource
    Online Resource
    Pentazocine: Hemodynamic and Electrophysiologic Properties
    Wiley ; 1973
    In:  The Journal of Clinical Pharmacology and New Drugs Vol. 13, No. 8-9 ( 1973-08-09), p. 313-324
    Details
    In: The Journal of Clinical Pharmacology and New Drugs, Wiley, Vol. 13, No. 8-9 ( 1973-08-09), p. 313-324
    Type of Medium: Online Resource
    ISSN: 0021-9754
    URL: Issue
    URL: Article
    DOI: 10.1002/jcph.1973.13.issue-8-9
    DOI: 10.1002/j.1552-4604.1973.tb00218.x
    RVK:
    XA 52835
    Language: English
    Publisher: Wiley
    Publication Date: 1973
    detail.hit.zdb_id: 2010253-7
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    Hemodynamic Spectrum of Myocardial Infarction and Cardiogenic Shock : A Conceptual Model
    Ovid Technologies (Wolters Kluwer Health) ; 1972
    In:  Circulation Vol. 45, No. 5 ( 1972-05), p. 1097-1110
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. 5 ( 1972-05), p. 1097-1110
    Abstract: Despite the recent accumulation of a large hemodynamic data base describing myocardial infarction and cardiogenic shock, precise characterization of patient subsets has been elusive. This paper represents an attempt to identify the major factors contributing to this wide hemodynamic spectrum, and their interrelation using a theoretical model based upon currently emerging concepts of this disease. It is proposed that the hemodynamic alterations associated with acute infarction are a consequence both of reduction in contractile mass and alteration in left ventricular compliance. In addition, mitral insufficiency, altered contractility, and the peripheral circulation interact to produce wide divergence between clinical and hemodynamic features from case to case and during the progression of the course of the illness. This model may more rationally explain the genesis and natural history of "heart failure" and the "shock syndrome" associated with acute myocardial infarction and in addition explain the extremely variable responses to both drug therapy and to more aggressive modes of treatment of power failure.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.45.5.1097
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1972
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  • 5
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    Online Resource
    Assessment of Passive Elastic Stiffness for Isolated Heart Muscle and the Intact Heart
    Ovid Technologies (Wolters Kluwer Health) ; 1973
    In:  Circulation Research Vol. 33, No. 2 ( 1973-08), p. 233-243
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 2 ( 1973-08), p. 233-243
    Abstract: A sensitive method was developed for detecting stiffness changes in the left ventricle. Stress-strain relationships (σ--ε) were obtained in the form dσ/dε = kσ + c from published studies on eight normal canine hearts, five infarcted canine hearts, and seven isolated cat papillary muscles. Utilizing pressure-volume relationships, the elastic stiffness (dσ/dε) and the stiffness constant ( k ) were also evaluated in patients with normal ventricles, inappropriate hypertrophy, and congestive cardiomyopathy. The k values were 35.0 ± 1.7 (isolated muscle, 30°C), 37.3 ± 1.9 (normal canine, 23°C), and 23.9 (infarcted). For the patient groups, k and the passive elastic stiffness were 15.8 ± 0.3 and 249 ± 22.4 g/cm 2 for 13 normal patients, 26.4 ± 1.7 and 286 ± 32.0 g/cm 2 for 7 patients with inappropriate hypertrophy, and 20.1 ± 1.2 and 1360 ± 209 g/cm 2 for 6 patients with congestive cardiomyopathy. The results indicate that (1) k is sensitive to stiffness changes due to infarction, (2) hypertrophy causes an increase in the value of k although elastic stiffness remains within normal limits, and (3) k for the intact human heart is lower than it is for isolated muscle.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.33.2.233
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1973
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    Series Elasticity in Heart Muscle : Its Relation To Contractile Element Velocity And Proposed Muscle Models
    Ovid Technologies (Wolters Kluwer Health) ; 1967
    In:  Circulation Research Vol. 20, No. 1 ( 1967-01), p. 112-123
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 1 ( 1967-01), p. 112-123
    Abstract: The series elasticity (SE) of cat papillary muscle was measured in 6 muscles by the isotonic quick-release method, with careful correction for the compliance of the equipment. The resultant SE curve was exponential in form with an extension of 4% to 5% of initial muscle length for a preload of 0.5 g and a developed tension of 10 g; this demonstrates a stiffer SE for cardiac muscle than has previously been reported. The quick-release SE extension curve was unaffected by inotropic interventions or changing the time of quick release, and was less compliant than the SE curves calculated by two different isotonic methods. These differences arise from the fact that contractile element velocity has a secondary rise during the transition from the isometric to isotonic phase of any afterloaded contraction. With increasing preload (and initial muscle length) the SE became stiffer, suggesting that a substantial part of it is in series with both the contractile and parallel elastic elements.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.20.1.112
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1967
    detail.hit.zdb_id: 1467838-X
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  • 7
    Online Resource
    Online Resource
    Silent Mitral Insufficiency in Acute Myocardial Infarction
    Ovid Technologies (Wolters Kluwer Health) ; 1971
    In:  Circulation Vol. 44, No. 5 ( 1971-11), p. 877-883
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. 5 ( 1971-11), p. 877-883
    Abstract: Severe mitral insufficiency in the absence of an audible murmur was diagnosed by left ventricular angiography in three patients with power failure secondary to acute myocardial infarction during evaluation for mechanical circulatory assist and surgery. Mitral valve prolapse was present in two patients. Postmortem examination did not reveal an anatomic basis for the mitral insufficiency: the valve, papillary muscles, and supporting structures were all grossly normal. A single papillary muscle removed at surgery revealed a marked decrease in force development (0.22 g/mm 2 vs 0.62 ± 0.22 g/mm 2 in eight normal papillary muscles from patients with rheumatic heart disease). During isoproterenol stimulation, force development in this muscle decreased 20%, whereas in the normal muscles force development increased 73 ± 31%. Microscopically, all papillary muscles revealed evidence of extensive necrosis. Silent mitral insufficiency in acute myocardial infarction, therefore, was probably related to diminished flow velocity across the mitral valve secondary to diminished myocardial contractility. Failure to recognize and treat this entity may contribute significantly to the genesis of power failure and ultimate mortality.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.44.5.877
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1971
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  • 8
    Online Resource
    Online Resource
    An Analysis of Segmental Ischemic Dysfunction Utilizing the Pressure-Length Loop
    Ovid Technologies (Wolters Kluwer Health) ; 1974
    In:  Circulation Vol. 49, No. 4 ( 1974-04), p. 748-754
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 49, No. 4 ( 1974-04), p. 748-754
    Abstract: Left ventricular (LV) pressure and myocardial segment length, determined by an epicardial mercury-in-silastic length gauge, were plotted simultaneously to obtain a pressure-length loop before and after left anterior descending artery (LAD) occlusion in 11 dogs. Previous studies have indicated that the area within this loop is a sensitive and reproducible means of quantitating regional myocardial performance. Immediately following ligation, systolic performance deteriorated as indicated by progressive reduction in the pressure-length loop area. Within approximately 30 sec a zero area for the pressure-length loop was observed, indicating no effective work was being performed by the ischemic segment. During the ensuing 3-5 min the pressure-length loop moved into a clockwise orientation which indicated work was being done on rather than by the segment. The magnitude was approximately 50% of that amount previously generated by the segment. In addition, during this latter period of repetitive passive stretch, the end-diastolic pressure-length relationship shifted to the right indicating increased diastolic compliance. Restoration of perfusion after 30 min produced variable results. Substantial return of function was observed in two animals, but recovery in the majority of animals was limited to the elimination of paradoxical expansion without restoration of active contraction. Therefore, the pressure-length loop method allows quantitation of regional myocardial performance, and indicates that a predictable pattern of significant changes in both systole and diastole accompanies acute myocardial ischemia.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.49.4.748
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1974
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  • 9
    Online Resource
    Online Resource
    Depression of Myocardial Contractility in Rats by Free Fatty Acids during Hypoxia
    Ovid Technologies (Wolters Kluwer Health) ; 1970
    In:  Circulation Research Vol. 26, No. 4 ( 1970-04), p. 439-449
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 26, No. 4 ( 1970-04), p. 439-449
    Abstract: Rat papillary muscles were used to study the influence of glucose (5 m M ), linoleate (1 to 1.75 m M ), octanoate (0.5 to 1.75 m M ) and pent-4-enoic acid (1 to 5 m M ) on mechanical performance under oxygenated, hypoxic and anoxic conditions. The buffer solution contained 0.3 m M albumin. Free fatty acids (FFA) (1.0 to 1.75 m M ) did not alter mechanical performance under oxygenated conditions. During hypoxia or anoxia, FFA (0.5 to 1.75 m M ) depressed contractility and increased resting force; glucose improved mechanical performance and modified the depressant effects of FFA. The depressant effect of the nonmetabolized FFA, pentenoic acid, was similar to that of other FFA. This suggests that the effect was mediated directly by FFA or acyl CoA derivatives rather than their metabolic products, and that it might be due to a detergent effect or calcium binding by FFA present in excess of intracellular FFA binding capacity at low pH. Force development during anoxia could be augmented by calcium, implying that the reduced ability of the myofilaments to contract could not be attributed entirely to a reduction of high energy stores.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.26.4.439
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1970
    detail.hit.zdb_id: 1467838-X
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  • 10
    Online Resource
    Online Resource
    Effects of Glucagon on Myocardial Oxygen Consumption and Coronary Blood Flow in Man and in Dog
    Ovid Technologies (Wolters Kluwer Health) ; 1970
    In:  Circulation Vol. 41, No. 4 ( 1970-04), p. 579-588
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. 4 ( 1970-04), p. 579-588
    Abstract: The effects of intravenous administration of glucagon (50 µg/kg) on left coronary blood flow and myocardial oxygen consumption were studied in nine patients during diagnostic cardiac catheterization and in six open-chested anesthetized dogs. Coronary blood flow was measured with the 133 Xe washout technic in man, and with an electromagnetic flowmeter placed around the left anterior descending coronary artery in the dogs. In the patients, glucagon produced a 31% increase in coronary blood flow and a 29% increase in myocardial oxygen consumption, with no change in coronary arteriovenous (A-V) O 2 difference across the heart. In the dogs glucagon produced a 114% increase in coronary blood flow and a 131% increase in myocardial oxygen consumption, again with no change in coronary A-V O 2 difference. Thus glucagon is a secondary coronary vasodilator in both man and dog. The modest chronotropic and inotropic effects of glucagon observed in man were only half as great as those observed in the dog. Part or all of this difference in dose-response relationship between the two species may be related to the different experimental conditions of the study.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.41.4.579
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1970
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