Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was evaluation of intravenous propafenone hydrochloride effects on maintenance of atrial signal-averaged ECG (ASAECG) during time-domain and frequency-domain analyses in patients paroxysmal atrial fibrillation (PAF) accompanying ischemic heart disease (IHD). The study population of 20 patients included 12 women and 8 men (mean age 58.8 +/- 8.9). For ASAECG were calculated time-domain parameters: the root mean square voltage of the signals in the last 10, 20, 30 ms of the filtered P-wave (RMS 10, 20, 30) and duration of filtered P-wave (PWD). During frequency-domain analysis of the terminal part of P-wave the following parameters were calculated in the range from 40 Hz to 400 Hz: energy spectrum > -60 dB (A, YA) and decibel drop at 40 Hz (Dd, YDd) in logarithmic scale and area ratio 20-50/0-20 Hz (Ar, YAr), peak (P1-7, YP1-7), magnitude ratio (MR1-7, YMP1-7) in linear scale for a vector magnitude and Frank lead Y. Time-domain analysis of ASAECG did not show any significant changes--RMS10 increased from 5.2 +/- 2.5 microV to 5.9 +/- 2.6 microV, RMS20 from 6.9 +/- 3.4 microV to 7.3 +/- 2.5 microV and RMS30 from 8.4 +/- 3.1 microV to 8.5 +/- 2.2 microV after propafenone. Duration of filtered P-wave (PWD) increased from 125.1 +/- 21.9 ms to 128.4 +/- 22.7 ms (p > 0.05). During frequency-domain analysis both in linear and logarithmic scales no any significant differences after administration of propafenone were noted. The obtained results have indicated that intravenous propafenone hydrochloride did not change significantly time-domain and frequency-domain parameters of ASAECG in patients with PAF during IHD.
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PMID:[Effect of intravenous propafenone on maintenance of atrial signal-averaged ECG in patients with paroxysmal atrial fibrillation]. 892 47

Recording of ventricular signal-averaged ECG (VSAE) were carried out in 19 patients suffering from ischemic heart disease before and after intravenously administration of amiodarone using a commercially available machine HIPEC-200 HA device of Aerotel's. The high gain ECG was recorded during basic rhythm with orthogonal Frank leads X, Y, Z. These combined into a vector magnitude and the QRS duration (QRS), the duration of low amplitude signals < 40 microV (LPD) and the root mean square voltage of the signals in the last 40 and 50 ms of the filtered QRS (RMS 40,50) were calculated for VSAE. It was time-domain analysis of VSAE. In frequency domain analysis were calculated the following parameters in range from 40 Hz to 400 Hz in linear scale: area ratio 20-50 Hz/0-20 Hz, peak and magnitude ratio and in logarithmic scale: energy spectrum > -60 dB and decibel drop at 40 Hz. Subsequently amiodarone hydrochloride was given intravenously 5 mg/kg c.c. and again time-domain and frequency domain analysis were done. Data presented are mean +/- standard deviation. Statistical comparisons were performed with paired t-Student test. Significance refers to a p values < 0.05. Time-domain analysis of VSAE didn't show any significant differences after amiodarone injection. During frequency-domain analysis of VSAE statistically significant differences were displayed in Frank lead X and Y for energy spectrum > -60 dB. In Frank lead X decrease of this parameter after amiodarone (from 3322 +/- 1057 dB-Hz to 2628 +/- 733) and in lead Y increase (from 2793 +/- 500 dB-Hz to 3199 +/-938 dB-Hz) was noticed. Our observation have indicated that intravenously application of amiodarone hydrochloride didn't change parameters in time-domain analysis. Statistically significant differences were noticed only during frequency analysis VSAE in logarithmic scale -energy spectrum > -60 dB but only in two leads X and Y.
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PMID:[The effect of intravenously given amiodarone on maintenance of ventricular signal averaged electrocardiogram in patients with ischemic heart disease]. 892 46

The aim of this study was to assess the correlation between left atrial size and atrial signal-averaged electrocardiogram (ALP) in time-domain and frequency analysis in patients with paroxysmal atrial fibrillation (PAF) during ischaemic heart disease (IHD). The study population consisted of 75 patients with PAF during IHD who were divided into two groups; gr. I (left atrial dimension 40 mm) and gr. II (left atrial dimension 40 mm). The control group (gr. III) consisted of 50 healthy subjects. Recording of ALP was carried out by HIPEC-200HA. The high gain ECG was recorded during basic rhythm with orthogonal Frank leads X,Y,Z. These signals were amplified, averaged and filters. The filtered signals were combined into a vector magnitude and time-domain and frequency analysis was done. These findings suggest that the size of the left atrium does not change time-domain and frequency parameters of ALP in patients with PAF and IHD. We noticed significant influence of IHD on these parameters. On the other hand frequency analysis of ALP did not show any uselessness in diagnostic identification of patients with PAF during IHD and healthy subjects.
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PMID:[Correlations between left atrial size and parameters of averaged atrial signal in patients with paroxysmal atrial fibrillation in the course of ischemic heart diseases]. 915 25

The aim of this study was to evaluate of oral sotalol hydrochloride effects on atrial signal-averaged ECG (ASAECG) during time- and frequency-domain analysis in patients with paroxysmal atrial fibrillation (PAF) during ischemic heart disease (IHD). The study population of 27 was composed of 16 female and 11 male, mean age 56.1 +/- 8.4. The dose of oral sotalol was 160 mg/day for all days. Recording of ASAECG and 24-hours Holter monitoring were made at baseline, after 10 days and after 6 weeks of sotalol therapy. For ASAECG were calculated time-domain parameters: the root mean square voltage of the signals in the last 10, 20, 30 ms of the filtered P-wave (RMS 10, 20, 30) and total time duration of filtered P-wave (PWD) and time duration of P-wave for Frank leads X, Y, Z (XP, YP, ZP). During frequency-domain analysis of the terminal part of P-wave we calculated the following parameters in range from 40 Hz to 400 Hz: energy spectrum > -60 dB (A) and decibel drop at 40 Hz (Dd) in logarithmic scale and area ratio 20-50/0-20 Hz (Ar), magnitude ratio (MR1-7) in linear scale for a vector magnitude. Supraventriculat arrhythmias were estimated quantitatively and qualitatively during Holter monitoring. The following parameters were estimated in a case of PAF recording: time of manifestation, duration, number of PAF episodes per day, mean heart rate during PAF and subjective symptoms. Moreover, comparable analysis of the following parameters: dimension of left atrial, age, gender, time duration of IHD and PAF and wall motion disturbances-hypokinesis and also left ventricular ejection fraction, mitral regurgitation was done between patients with effective and no effective of antiarrhythmic therapy. Our observation have indicated that oral sotalol therapy are responsible for statistically significant decrease of total time duration of filtered P-wave (PWD) and time duration of P-wave for Frank leads X, Y, Z (XP, YP, ZP) and increase area ratio 20-50/0-20 Hz in patients with PAF during IHD. Moreover, comparable analysis of above-mentioned parameters have not showed statistically significant differences between examined patients with effective and lack of effective sotalol therapy.
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PMID:[The effect of sotalol hydrochloride therapy on atrial signal-averaged ECG in patients with paroxysmal atrial fibrillation]. 927 1

Microvolt-level T-wave alternans (alternating morphology from beat to beat) during atrial pacing and exercise may predict ventricular tachycardia (VT) and fibrillation (VF) in ischemic heart disease. We tested whether such alternans during exercise could identify high-risk patients with hypertrophic cardiomyopathy (HCM). We studied 14 HCM patients and 9 normal control subjects for T-wave alternans u sing the CH2000 system with 7 multisegment electrodes in a Frank orthogonal (XYZ) configuration. Bicycle ergometer exercise was used to increase the heart rate (HR) to 95-110 beats/min. Seven patients were at high risk for ventricular arrhythmias (1 with sustained VT, 3 with abnormal paced ventricular electrograms as seen in VF survivors, and 3 with nonsustained VT and/or an adverse family history), and the other 7 were at low risk. T-wave alternans was present if alternans > 1.9 microV was consistently present with the HR in excess of a patient-specific HR threshold. Alternans was found in 5 of 7 high-risk patients (71%) vs none of 7 low-risk patients or 9 control subjects (p < 0.025 and p < 0.01, respectively). Notably, all 4 patients with sustained VT or abnormal ventricular electrograms showed alternans. Thus, high-risk patients with HCM often show T-wave alternans. Microvolt-level alternans during exercise may be a useful marker for ventricular arrhythmic risk in patients with HCM.
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PMID:Exercise-induced T-wave alternans as a marker of high risk in patients with hypertrophic cardiomyopathy. 927 69

Chronic myocardial ischemia is the leading cause of disturbances in myocardial contractility (myocardial infarction) or hemodynamic overload upon the left ventricle. The heart reactions consist in a series of adaptative mechanisms in order to maintain its pump function: Frank-Starling mechanism, myocardial hypertrophy and neurohumoral activation. In heart failure, the cardiac output is maintained by an increase of the preload which enhances the contractility (Frank-Starling law). Myocardial ischemia influences the systolic and diastolic function. The decrease of cardiac output leads to neurohumoral responses which, in the initial stages of cardiac failure are compensatory; along with the progression of the disease, they exert adverse effects. Increased activity of the sympathetic nervous system induces high cardiac rates, chronotropic incompetence. Activation of the renin-angiotensin system held to myocardial and vascular hypertrophy, vasoconstriction, fluid retention. Endothelin is the most powerful vasoconstrictor; its plasmatic concentrations correlate with the severity of the disease. Vasodilator mediators released in cardiac failure are the natriuretic peptide, nitric oxide, dopamine, prostacicline, bradikinin.
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PMID:[Heart failure due to ischemia--the adaptive mechanisms]. 1075 79

It is now clear that diastolic heart failure (DHF) is an important, perhaps even dominant form of heart failure in older Americans. However, our knowledge base regarding the epidemiology, pathophysiology, natural history, and therapy of this relatively recently recognized disorder is limited. A number of normal age related changes in the heart and vascular system may predispose to or lower the threshold for expression of DHF. Recent reports from large population-based observational studies indicate that over 50% of persons 65 years and older who have heart failure have normal LV systolic function (presumed DHF). Among these, 45% have no other confounding variables (coronary, valvular, or pulmonary disease) and meet the criteria for isolated DHF. DHF is substantially more common in older women than men. A history of systemic hypertension and left ventricular hypertrophy are almost invariably present. Mortality rates are about 50% lower in DHF than in systolic heart failure (SHF) when stable outpatients are considered. However, in hospitalized and very elderly patients, the mortality rate appears similar in DHF and SHF. Furthermore, due to its higher prevalence, the total mortality in the older population attributable to DHF exceeds that of SHF. Morbidity in DHF is substantial and approaches that of SHF. In the chronic setting, DHF patients can have severe exercise intolerance related to failure of the Frank-Starling mechanism with reduced peak cardiac output, heart rate, and stroke volume and increased LV filling pressure. DHF patients also appear to have increased vascular stiffness, accelerated systolic blood pressure response to exercise, neuroendocrine activation, and reduced quality of life. Acute exacerbations (pulmonary edema) frequently occur and are associated with severe hypertension, sodium indiscretion, and medication non-compliance. Surprisingly, overt myocardial ischemia appears to infrequently play a role in these acute exacerbations. Therapy is currently empiric and multicenter, randomized, controlled trials are urgently needed. Anecdotally, control of blood pressure appears to improve symptoms and reduce the frequency of acute exacerbations. In addition, non-pharmacologic intervention, including multi-disciplinary case management is useful.
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PMID:Diastolic heart failure in the elderly. 1179 Sep 20

In acute coronary syndromes, GPIIb/IIIa platelet inhibitors have demonstrated a reduction in recurrent myocardial ischemia. Conversely, one might expect that enhancing platelet activity in patients in acute coronary syndromes would have the opposite effect. We report a patient with idiopathic thrombocytopenic purpura (ITP) that had recurrent myocardial ischemia associated with administration of intravenous immunogloblin (IVIG). Literature is reviewed.
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PMID:Intravenous immunoglobulin-related acute coronary syndrome and coronary angiography in idiopathic thrombocytopenic purpura--a case report and literature review. 1186 4

The EASI lead system, which is based on the dipole hypothesis of vectorcardiography, offers the possibility of deriving the standard 12-lead electrocardiogram (ECG) and other desired leads from ECGs recorded at only 4 sites; it uses the Frank E, A, and I electrode locations, a fourth electrode location (S) at the manubrium, and a reference electrode. Accordingly, the electrodes of this system can be applied rapidly on easy-to-locate, stable anatomical sites that leave the precordium free for other diagnostic procedures. In early EASI implementations, the derived leads differed from actual leads by more than some clinicians found acceptable. As these differences were thought to be caused by the fact that the coefficients that were used had been derived from a limited data set, we have calculated a new set of EASI coefficients for the standard 12 leads, and several other leads, by using a data set of 983 adult subjects with 120-lead ECGs and well-documented diagnoses. This database is a concatenation of 2 previously described ones: one consisting of 892 persons (normal subjects, postmyocardial-infarction patients with and without arrhythmias, and patients with ventricular arrhythmias but no history of myocardial infarction) and the other consisting of 91 patients with single-vessel coronary artery disease who underwent coronary balloon-inflation angioplasty. In addition to the coefficients for the standard 12 leads (derived for standard limb leads as well as for Mason-Likar leads), we derived coefficients for six additional unipolar leads (posterior V(7)-V(9), and right-sided V(3)R-V(5)R), the Frank orthogonal leads, and three bipolar, vessel-specific leads that have been previously shown to exhibit optimal sensitivity for acute myocardial ischemia. We also derived coefficients for the modified electrode locations of the EASI system that must be used with patients who have undergone a midline sternotomy. Optimal coefficients for lead transformations were determined by maximizing the ensemble average (over the entire data set) of the correlation between the derived and the true lead for the chosen interval of the averaged complex. For derived standard limb leads, the amplitude was adjusted to give the best root-mean-square fit over the entire PQRST interval, whereas for derived Mason-Likar leads it was adjusted to give the best ST-segment fit. The entire set of coefficients and their corresponding goodness-of-fit measures are presented.
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PMID:Improved EASI coefficients: their derivation, values, and performance. 1253 96

Peroxisome proliferator-activated receptor (PPAR)-gamma modulates substrate metabolism and inflammatory responses. In experimental rats subjected to myocardial ischemia-reperfusion (I/R), thiazolidinedione PPAR-gamma activators reduce infarct size and preserve left ventricular function. Troglitazone is the only PPAR-gamma activator that has been shown to be protective in I/R in large animals. However, because troglitazone contains both alpha-tocopherol and thiazolidinedione moieties, whether PPAR-gamma activation per se is protective in myocardial I/R in large animals remains uncertain. To address this question, 56 pigs were treated orally for 8 wk with troglitazone (75 mg x kg(-1) x day(-1)), rosiglitazone (3 mg x kg(-1) x day(-1)), or alpha-tocopherol (73 mg x kg(-1) x day(-1), equimolar to troglitazone dose) or received no treatment. Pigs were then anesthetized and subjected to 90 min of low-flow regional myocardial ischemia and 90 min of reperfusion. Myocardial expression of PPAR-gamma, determined by ribonuclease protection assay, increased with troglitazone and rosiglitazone compared with no treatment. Rosiglitazone had no significant effect on myocardial contractile function (Frank-Starling relations), substrate uptake, or expression of proinflammatory cytokines during I/R compared with untreated pigs. In contrast, preservation of myocardial contractile function and lactate uptake were greater and cytokine expression was attenuated in pigs treated with troglitazone or alpha-tocopherol compared with untreated pigs. Multivariate analysis indicated that presence of an alpha-tocopherol, but not a thiazolidinedione, moiety in the test compound was significantly related to greater contractile function and lactate uptake and lower cytokine expression during I/R. We conclude that PPAR-gamma activation is not protective in a porcine model of myocardial I/R. Protective effects of troglitazone are attributable to its alpha-tocopherol moiety. These findings, in conjunction with prior rat studies, suggest interspecies differences in the response to PPAR-gamma activation in the heart.
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PMID:PPAR-gamma activation fails to provide myocardial protection in ischemia and reperfusion in pigs. 1552 32


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