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PubMed1984

Noninvasive assessment of acute effects of nifedipine on rest and exercise hemodynamics and cardiac function in patients with aortic regurgitation.

The acute effects of nifedipine (20 mg sublingually) on hemodynamics and cardiac function were studied at rest and during supine bicycle exercise in 20 patients with aortic regurgitation. At rest, heart rate increased by 13%, systemic vascular resistance decreased by 34% and regurgitant index decreased by 17%. The change in systemic vascular resistance was related to its initial rest level (r = 0.82, p less than 0.001) and to the changes in forward cardiac output (r = 0.58, p less than 0.01) and regurgitant index (r = 0.60, p less than 0.01). Left ventricular end-diastolic and end-systolic volumes, stroke volume and ejection fraction were unchanged, whereas right ventricular ejection fraction increased. During exercise, nifedipine administration further increased heart rate by 8% and decreased systemic vascular resistance by 19%. Both forward stroke volume and forward cardiac output increased, but total left ventricular stroke volume was unchanged, resulting in a significant decrease in regurgitant index. Although left ventricular end-diastolic volume was slightly decreased, end-systolic volume did not increase; thus, ejection fraction was higher than that during control exercise (p less than 0.01). Right ventricular ejection fraction increased further. In aortic regurgitation, the acute administration of nifedipine improved cardiac performance and reduced regurgitation at rest and during exercise as a result of afterload reduction and increased heart rate. Whether these beneficial effects will occur during long-term therapy requires further investigation.

Adult↗

PubMed1985

Relation of hemoglobin A1 and blood glucose to cardiac function in diabetes mellitus.

To examine the relation of short- and long-term changes in glucose metabolism to cardiac function, radionuclide cineangiography and echocardiography were performed in 10 young insulin-dependent diabetic patients without clinical evidence of heart disease. Cardiac assessments were performed before and after both acute variations in blood glucose, and induction of chronic "tight glucose control" involving normalization of hemoglobin A1 concentrations. In diabetic patients, left ventricular (LV) ejection fraction (EF) at normal blood glucose concentration was indistinguishable from values in 11 normal subjects. However, during hyperglycemia (about 300 mg/dl), the average EF at rest was 61%, significantly higher than that during normoglycemia (56%, p less than 0.001). No significant change in LV diastolic dimension was noted in association with shifts between high and normal blood glucose concentrations. Normalization of hemoglobin A1 was achieved within 6 to 25 weeks. This alteration had no significant effect on LVEF, mitral valve E-F slope, or the response of systolic function to blood glucose levels. In addition, no correlation was found between LVEF and hemoglobin A1 concentrations in 4 of 5 evaluation periods. Thus, in young insulin-dependent diabetic patients without overt heart disease, variation in blood glucose concentration is associated with small but significant variation in EF at rest; normalization of hemoglobin A1 has no significant effect on LVEF or the response of systolic function to blood glucose levels.

Adult↗

PubMed1996

[Assessment of cardiac functions in patients for coronary artery bypass graft using transesophageal echocardiography before and after cardiopulmonary bypass].

We evaluated cardiac functions in 7 patients for elective coronary artery bypass graft surgery before and after cardiopulmonary bypass (CPB) using transesophageal echocardiography (TEE). There was no significant difference in the ratio of end-systolic meridional wall stress (ESS) and end-systolic area (ESA), which is a good indicator of cardiac contractility, before and after CPB period. However, left ventricular stroke work index (LVSWI) decreased after CPB compared to that before CPB. There was a positive correlation between the ESS/ESA ratio after induction of anesthesia and left ventricular ejection fraction at the pre-operative study. As the ESS/ESA ratio represents cardiac contractility and the ESS is a reliable indicator of afterload, we thought it possible to assess cardiac contractility and precise afterload by using TEE during perioperative period.

Aged↗

PubMed1987

The effects of dietary mackerel oil on the recovery of cardiac function after acute ischaemic events in the pig.

To investigate the effects of fish oil nutrition on cardiac haemodynamics and the biochemical response to ischaemia-reperfusion, young pigs (5 weeks old) were fed a 9% lard fat diet or a mixed diet of 4.5% mackerel oil and 4.5% lard fat for 16 weeks. In the mackerel oil fed pigs plasma cholesterol and triglyceride levels decreased by 22% and 58% (both p less than 0.05), respectively, while levels in the animals which received only lard fat did not change. The n-6 fatty acids present in cardiac and platelet membrane phospholipids underwent a partial replacement by n-3 fatty acids in the mackerel oil fed pigs. Under anaesthesia, multiple coronary artery occlusions (5 min) were interrupted by 10 min of reperfusion. The extent of recovery of cardiac function and reduction of adenine nucleotide levels were similar for both dietary groups. The incidence of reperfusion arrhythmias was significantly lower and the reactive hyperaemic responses were of longer duration in the mackerel oil fed animals. These effects cannot be explained by diet-induced alterations in thromboxane B2/6-keto-PGF1 alpha ratio, although a marked reduction in absolute levels of both prostaglandins was seen in the mackerel oil fed pigs (p less than 0.05). In conclusion, dietary fish oil caused changes in membrane fatty acid composition and plasma prostaglandin levels, although these did not affect alterations of cardiac performance during and after short periods of ischaemia.

Animals↗

PubMed2003

Model of functional cardiac aging: young adult mice with mild overexpression of serum response factor.

Serum response factor (SRF) is an important transcription factor that may have a role in the maintenance of cardiac structure and function. The level of SRF mRNA expression increases approximately 16% in the hearts of mice during adult aging. To model the effect of mild SRF elevation in the aging heart, transgenic mice with low levels of SRF overexpression were generated. By 6 mo of age, the transgenic mice had a 19% increase of heart-to-body weight ratio compared with nontransgenic mice. In addition, they had a 12% increase in myocyte size, a 6.7% increase in collagen deposition, and altered gene expression of a number of muscle-specific and cardiac genes. Doppler echocardiography revealed that these transgenic mice had increased left ventricular wall thickness and decreased left ventricular (LV) volumes, increased LV stiffness with 20% reduction in early diastolic LV filling (peak E), and 35% decline in peak E-to-peak A (late diastolic filling) ratio. The observed changes, especially those in the E/A ratio, are similar to those seen clinically in late life as a part of human adult myocardial aging.

Aging↗

PubMedDate not supplied

Protective effect of glutamic acid on cardiac function and metabolism during cardioplegia and reperfusion.

The effect of glutamic acid added to cardioplegic solution containing 20 mM K+ on the cardiac function and metabolism was studied in isolated working rat hearts. 30-min cardiac arrest resulted in profound fall in creatine phosphate and ATP content, by four- and two-fold, respectively, as well as in four-fold rise in AMP content. Simultaneously, during cardioplegia a decline in tissue glutamate and aspartate content and an increase in tissue ammonia and alanine content were found. After reperfusion, an incomplete restoration of ATP, AMP, and creatine phosphate content were observed; the cardiac output recovered only to 39 percent of the initial value. An addition of glutamic acid to cardioplegic solution was associated with significantly less decline in the content of high-energy phosphates and less prominent rise in AMP content during cardioplegia. It also prevented the decline in tissue aspartate content and caused a lesser ammonia accumulation in myocardial tissue due to the activation of glutamine synthesis. In spite of this the tissue ammonia level remained elevated. Reperfusion with Krebs-Henseleit buffer resulted in the recovery of cardiac output to 75% of the initial value as well as better restoration of high-energy phosphate content. The addition of glutamic acid in the perfusate during reperfusion led to further improvement of ATP and creatine phosphate content. It is suggested that an addition of glutamic acid may have beneficial effect in open heart surgery.

Adenine Nucleotides↗

PubMed1987

Influence of diltiazem on cardiac function at organ and molecular level during hypothermic cardiac arrest.

The present study was undertaken to assess the effects of cold crystalloid cardioplegia with and without diltiazem on the functional recovery of the heart, calcium binding and uptake by the sarcoplasmic reticulum, Ca++ATPase of sarcoplasmic reticulum and coronary sinus serum MBCK (MB fraction of creatine kinase) of dogs, after 1.5 h of reperfusion following 1 h of ischemic cardiac arrest. The dogs were divided into three groups: group I, sham bypass (no ischemic cardiac arrest); group II, cold crystalloid cardioplegia; group III, cold crystalloid cardioplegia with diltiazem. The results showed that the decrease in the index of cardiac contractility and cardiac index which accompanies cold crystalloid cardioplegia is associated with a decrease in the calcium uptake by sarcoplasmic reticulum. The index of myocardial contractility was better preserved with cold crystalloid plus diltiazem than with cold crystalloid alone. This improvement, although partial, in cardiac contractility with cold crystalloid plus diltiazem, was associated with a tendency for an increase towards control values in the calcium uptake by sarcoplasmic reticulum. There were no changes in Ca++ATPase of, and calcium binding by, the sarcoplasmic reticulum of groups II and III when compared to group I. There was a progressive increase in the MBCK of coronary sinus blood in groups II and III. The MBCK of group I was unchanged throughout the experimental protocol. The increases in the MBCK of coronary sinus blood were less in group III than in group II indicating the protective effect of diltiazem on ischemic and reperfusion myocardial injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Cardiac function in patients with human immunodeficiency virus infection and with no other active infections.

OBJECTIVE: to investigate cardiac function and prognostic significance of echocardiographic findings in patients with uncomplicated human immunodeficiency virus (HIV)-infection. PATIENTS AND METHODS: Doppler echocardiography was performed in 60 male patients with HIV-infection and no signs of other active infections, and in 36 age and sex matched normal control subjects. The survival time of the patients was assessed 36 months after the echocardiographic examination. RESULTS: None of the patients had significant pericardial effusions, intracardiac tumors, signs of valvular endocarditis or dilated cardiomyopathy. In none of the patients were the fractional shortening or the early and atrial mitral flow ration (E/A ratio) below the 95% confidence limit of the control group. The E/A ratio was slightly, but significantly, decreased in AIDS patients both as compared to asymptomatic HIV-infected patients and as compared to normal control subjects because of increased heart rated in the AIDS patients. Within the three-year observation period, 28 of the patients died from HIV-related disease. In the group of deceased patients, there was no significant correlation between blood pressure, heart rate, left ventricular diameters, fractional shortening, E/A ratio and the survival time. CONCLUSION: In a population of HIV-infected patients with no other active infections, cardiac abnormalities seen to be uncommon, and the echocardiographic fractional shortening and E/A ratio were not related to the survival time of such patients. Thus, our data does not evidence that HIV is a direct cardiac pathogen.

Acquired Immunodeficiency Syndrome↗

PubMed2001

Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a genetic disease characterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (LV) dysfunction. We have proposed that hypertrophy and fibrosis, the major determinants of mortality and morbidity, are potentially reversible. We tested this hypothesis in beta-myosin heavy chain-Q(403) transgenic rabbits. METHODS AND RESULTS: We randomized 24 beta-myosin heavy chain-Q(403) rabbits to treatment with either a placebo or simvastatin (5 mg. kg(-1). d(-1)) for 12 weeks and included 12 nontransgenic controls. We performed 2D and Doppler echocardiography and tissue Doppler imaging before and after treatment. Demographic data were similar among the groups. Baseline mean LV mass and interventricular septal thickness in nontransgenic, placebo, and simvastatin groups were 3.9+/-0.7, 6.2+/-2.0, and 7.5+/-2.1 g (P<0.001) and 2.2+/-0.2, 3.1+/-0.5, and 3.3+/-0.5 mm (P=0.002), respectively. Simvastatin reduced LV mass by 37%, interventricular septal thickness by 21%, and posterior wall thickness by 13%. Doppler indices of LV filling pressure were improved. Collagen volume fraction was reduced by 44% (P<0.001). Disarray was unchanged. Levels of activated extracellular signal-regulated kinase (ERK) 1/2 were increased in the placebo group and were less than normal in the simvastatin group. Levels of activated and total p38, Jun N-terminal kinase, p70S6 kinase, Ras, Rac, and RhoA and the membrane association of Ras, RhoA, and Rac1 were unchanged. CONCLUSIONS: Simvastatin induced the regression of hypertrophy and fibrosis, improved cardiac function, and reduced ERK1/2 activity in the beta-myosin heavy chain-Q(403) rabbits. These findings highlight the need for clinical trials to determine the effects of simvastatin on cardiac hypertrophy, fibrosis, and dysfunction in humans with hypertrophic cardiomyopathy and heart failure.

Animals↗

PubMed1997

Global cardiac function using fast breath-hold MRI: validation of new acquisition and analysis techniques.

Calculation of global cardiac function parameters has been validated using fast, segmented k-space, breath-hold, gradient-echo, magnetic resonance images. Images of phantoms, experimental animals, normal volunteers, and patients were acquired with a 1.5 T clinical scanner. Humans were imaged using two phased-array surface coils in multicoil mode. Myocardial contours were extracted using a new interactive, semi-automated method based on the active contour model method. Images were acquired in the short-axis orientation, and, using a new imaging and analysis strategy, in rotating plane long-axis orientations, to provide better definition of the valve planes and the apex, and also to reduce the number of slices (compared with the short-axis method) required to sample the whole heart. Validation was accomplished through calculation of the volumes of phantoms and left and right ventricular masses of animal hearts. Functional parameters from MRI were compared with those from echocardiograms and radionuclide angiograms in normal volunteers and patients, respectively.

Adult↗

PubMed1989

Effects of terbutaline sulfate on fetal cardiac function.

An isolated heart preparation was used to study the effects of terbutaline sulfate (Brethine) on fetal cardiac function. Pregnant guinea pigs received daily subcutaneous injections of terbutaline for 10 day, whereas a control group received placebo injections. Fetal guinea pig hearts were evaluated for cariodynamic and pathologic differences. Fetuses exposed to terbutaline demonstrated a higher mean heart rate (p less than 0.01), a higher mean heart weight (p less than 0.05), a higher mean heart weight/body weight ratio (p less than 0.01), and a trend toward higher left ventricular systolic pressure levels (p less than 0.1). These hemodynamic responses in fetuses exposed to terbutaline may result in increased functional demands that may predispose myocardial tissue to damage.

Animals↗

PubMed2000

Modulation of mouse cardiac function in vivo by eNOS and ANP.

To study the role of endothelial nitric oxide synthase (eNOS) in cardiac function, we compared eNOS expression, contractility, and relaxation in the left ventricles of wild-type and eNOS-deficient mice. eNOS immunostaining is localized to the macro- and microvascular endothelium throughout the myocardium in wild-type mice and is absent in eNOS-/- mice. Whereas blood pressure is elevated in eNOS-/- mice, baseline cardiac contractility (dP/dt(max)) is similar in wild-type and eNOS-/- mice (9,673 +/- 2, 447 and 9,928 +/- 1,566 mmHg/s, respectively). The beta-adrenergic agonist isoproterenol (Iso) at doses of >/=1 ng causes enhanced increases in dP/dt(max) in eNOS-/- mice compared with wild-type controls in vivo (P < 0.01) as well as in Langendorff isolated heart preparations (P < 0.02). beta-Adrenergic receptor binding (B(max)) is not significantly different in the two groups of animals (B(max) = 41.4 +/- 9.4 and 36.1 +/- 5.1 fmol/mg for wild-type and eNOS-/-). Iso-stimulated ventricular relaxation is also enhanced in the eNOS-/- mice, as measured by dP/dt(min) in the isolated heart. However, baseline ventricular relaxation is normal in eNOS-/- mice (tau = 5.2 +/- 1.0 and 5.6 +/- 1.5 ms for wild-type and eNOS-/-, respectively), whereas it is impaired in wild-type mice after NOS inhibition (tau = 8.3 +/- 2.4 ms). cGMP levels in the left ventricle are unaffected by eNOS gene deletion (wild-type: 3.1 +/- 0.8 pmol/mg, eNOS-/-: 3.1 +/- 0.6 pmol/mg), leading us to examine the level of another physiological regulator of cGMP. Atrial natriuretic peptide (ANP) expression is markedly upregulated in the eNOS-/- mice, and exogenous ANP restores ventricular relaxation in wild-type mice treated with NOS inhibitors. These results suggest that eNOS attenuates both inotropic and lusitropic responses to beta-adrenergic stimulation, and it also appears to regulate baseline ventricular relaxation in conjunction with ANP.

Adrenergic beta-Agonists↗

PubMed1993

[Effect of percutaneous cardiopulmonary support (PCPS) on cardiac function with special reference to the significance of left ventricular venting].

Direct effects of percutaneous cardiopulmonary support (PCPS) on cardiac function were evaluated. Also, the efficacy of left ventricular venting to unload the heart was assessed. Eleven open-chested dogs were placed on PCPS with the flow equal to the baseline cardiac output for 30 minutes. Six out of eleven had left ventricle vented (VENT) by means of venting tube which was indwelt in the left ventricular cavity, while other five did not (NONVENT). Hemodynamic indices were obtained before and on PCPS. Measured, derived or calculated variables included heart rate (HR), mean aortic pressure (mean AOP), left ventricular end-diastolic pressure (LVEDP), peak left ventricular pressure (peak LVP), peak LVdp/dt, rate-pressure product (RPP, HR x peak LVP) and aortic-coronary sinus oxygen content difference (ACsO2D). There was no difference in any variables between the groups at baseline. On PCPS, in the VENT group, HR increased 27% from baseline (p < 0.05), while mean AOP did not change. All other variables showed significant (p < 0.05) reduction in VENT. Percent change from baseline value in VENT was: -24% for LVEDP, -47% for peak LVP, -41% for peak LVdp/dt, -32% for RPP and -42% for ACsO2D. No variable differed significantly from baseline in the NONVENT group on PCPS. The author concluded that left ventricular venting favorably alters the loading and contractile profile of the heart on PCPS without affecting systemic circulation.

Animals↗

PubMed2002

Decreased susceptibility of cardiac function to hypoxia-reoxygenation in renin-angiotensinogen transgenic rats.

We tested the hypothesis that the renin-angiotensin system (RAS) protects the contractile function of the myocardium against the damaging effect of hypoxia-reoxygenation. For this purpose, the contractility of isolated papillary muscles from wild-type (WT) rats and from rats expressing human renin and angiotensinogen as transgenes (TGR) was compared. After 15 min of hypoxia, peak force (PF) was decreased to 24 +/- 5% of the normoxic values in TGR (n = 10) and to 18 +/- 1% in WT rats (n = 12). PF and relaxation rates recovered completely in TGR but not in WT rats during 45 min of reoxygenation. Improved contractility of the papillary muscles from TGR during hypoxia-reoxygenation correlated with increased glutathione peroxidase activities and creatine kinase (CK)-MB and CK-BB isoenzyme levels. On the other hand, inhibition of the RAS with ramipril (1 mg/kg body wt for 3 wk) in WT animals resulted in deterioration of the contractile function of the papillary muscles during reoxygenation compared with untreated rats. These findings suggest that activation of the RAS protects contractile function of the cardiac muscle against hypoxia-reoxygenation, possibly through changes in CK isoenzymes and enhanced antioxidant capacity.

Animals↗

PubMed1986

Augmentation of cardiac function in end-stage heart failure by combined use of dobutamine and amrinone.

A patient with end-stage congestive cardiomyopathy had progressive hemodynamic deterioration while awaiting orthotopic heart transplantation. Attempts to support cardiovascular function by high-dose dobutamine infusions were complicated by life-threatening cardiac arrhythmias. The addition of the noncatecholamine inotropic agent, amrinone, improved ventricular performance, enabling reduction of the dose of dobutamine and resolution of the cardiac arrhythmias. Beta receptor stimulation by dobutamine combined with phosphodiesterase inhibition by amrinone may additively or synergistically augment cardiac function despite severe congestive heart failure and also have an adrenergic "sparing effect."

Aminopyridines↗

PubMed2001

The estimation of cardiac function from the rotary blood pump.

The rotary blood pump is implanted as a bridge to cardiac transplantation. Mechanical, histological, and biochemical improvements have been described in patients after implantation of left ventricular assist devices (LVADs). Thus, the rotary blood pump might be used as a bridge to recovery of myocardial function. However, unlike a pulsatile pump, the rotary blood pump cannot be stopped to estimate cardiac function: if the rotary blood pump stops, backflow will occur. In this study, a new method that can estimate cardiac function without pump stop was examined. Six pigs were the subjects of this acute study. The pump was implanted as an LVAD: the inlet cannula was inserted into the left ventricle, and the outlet cannula was inserted into the ascending aorta. The motor speed was regulated at a pump flow rate of 0 L/min at diastolic phase. Then, the relationship between the dp/dt of left ventricular pressure and external stroke work of actuator was examined. This method was studied at normal, hyperdynamic, and heart-failure conditions. There was a high positive correlation between the dp/dt of left ventricular pressure and external stroke work of actuator. This method is useful and simple to estimate cardiac function without pump stop.

Animals↗

PubMed1991

Beneficial effects of yohimbine on posthypoxic recovery of cardiac function and myocardial metabolism in isolated perfused rabbit hearts.

The present study was undertaken to elucidate the possible actions of yohimbine on cardiac function and metabolism in the hypoxic and subsequently reoxygenated myocardium. For this purpose, rabbit hearts were perfused for 20 min under hypoxic conditions, followed by 45 min reoxygenated perfusion, and their functional and metabolic alterations with and without yohimbine treatment were examined. Hypoxia induced cessation of cardiac contractile force, rise in resting tension and depletion of tissue high-energy phosphates, which were poorly recovered by subsequent reoxygenation. Hypoxia also induced release of creatine kinase and ATP metabolites from perfused hearts and increases in tissue calcium and sodium contents, which were further enhanced upon subsequent reoxygenation. When hypoxic hearts were treated with 3 to 30 microM yohimbine, several beneficial effects were observed in a concentration-dependent manner. This included enhancement of posthypoxic recovery of contractile function and suppression of the hypoxia- and reoxygenation-induced rise in resting tension. Hypoxia/reoxygenation-induced release of ATP metabolites was inhibited and restoration of myocardial high-energy phosphates enhanced. Inhibition of reoxygenation-induced rise in tissue calcium and sodium and creatine kinase release were also noted. The findings suggest that suppression of transmembrane flux of ions, substrates and enzymes during hypoxia/reoxygenation plays a role in the posthypoxic functional and metabolic recovery. Yohimbine (3-30 microM) significantly depressed the maximal stimulus frequency the left atria could follow. These results suggest a close relationship between depression in the maximal driving frequency of atria and enhancement of the posthypoxic contractile and metabolic recovery of perfused hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1995

Exacerbated tamponade: deterioration of cardiac function by lowering excessive arterial pressure in hypertensive cardiac tamponade.

Patients with cardiac tamponade usually have significant hypotension; hypertension is rare. Before administering any medication during tamponade one must consider the complex physiology and compensatory mechanisms of cardiac compression [1]. We observed both an accentuation of pulsus paradoxus and retrospectively recognized fluctuations of left-ventricular function after progressively rising arterial blood pressure had been lowered.

Antihypertensive Agents↗