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Biomedical subjects

R E Kleiger

Publications and source records attributed to R E Kleiger.

At least 19 recordsLinked to original sources
PubMed1992

Correlations among time and frequency domain measures of heart period variability two weeks after acute myocardial infarction.

Seven hundred fifteen participants from a multicenter natural history study of acute myocardial infarction were studied (1) to determine the correlations among time and frequency domain measures of heart period variability, (2) to determine the correlations between the measures of heart period variability and previously established post-infarction risk predictors, and (3) to determine the predictive value of time domain measures of heart period variability for death during follow-up after acute myocardial infarction. Twenty-four hour electrocardiographic recordings obtained 11 +/- 3 days after acute myocardial infarction were analyzed and 11 measures of heart period variability were computed. Each of 4 bands in the heart period power spectrum had 1 or 2 corresponding variables in the time domain that correlated with it so strongly (r greater than or equal to 0.90) that the variables were essentially equivalent: ultra low frequency power with SDNN* and SDANN index,* very low frequency power and low-frequency power with SDNN index,* and high-frequency power with r-MSSD* and pNN50.* As expected from theoretical considerations, SDNN and the square root of total power were almost perfectly correlated. Correlations between the time and frequency domain measures of heart period variability and previously identified postinfarction risk predictors, e.g., left ventricular ejection fraction and ventricular arrhythmias, are remarkably weak. Time domain measures of heart period variability, especially those that measure ultra low or low-frequency power, are strongly and independently associated with death during follow-up. * Defined in Table II.

Electrocardiography, Ambulatory↗
PubMed1992

The relationship between 1-year mortality and infarct location in patients with non-Q wave myocardial infarction.

The association between 1-year mortality and infarct location was evaluated in 544 patients with acute non-Q wave myocardial infarction. Infarcts were anterior (alone or including other locations) in 51.1% (n = 278) of cases, localizable but not anterior 29.6% (n = 161) of the time, and nonlocalizable in 19.3% (n = 105) of patients. One-year actuarial mortality (73 deaths) was 16.9% in the anterior group, 13.3% in the nonanterior group, and 6.8% in nonlocalizable patients (p = 0.037). Anterior and localizable nonanterior mortality were similar (p = 0.367). However, there were differences when mixed location infarcts were excluded. Mortality in the inferior infarction only group (2.8%, n = 36) was less than in the lateral infarction only group (16.8%, n = 79, p = 0.041) and almost significantly less than in the anterior only group (15.1%, n = 62, p = 0.064). The positive prognosis in the inferior infarction only group may be associated with the low rate of ST depression among these patients compared with those with other infarct locations (p less than 0.0001). Mortality among localizable infarcts (15.5%) was greater than among those that were nonlocalizable (6.8%, p = 0.021). Despite the low overall risk of the nonlocalizable infarcts, 41.9% (n = 44) of these patients developed at least one important risk factor while in hospital.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Frequency domain measures of heart period variability and mortality after myocardial infarction.

BACKGROUND: We studied 715 patients 2 weeks after myocardial infarction to establish the associations between six frequency domain measures of heart period variability (HPV) and mortality during 4 years of follow-up. METHODS AND RESULTS: Each measure of HPV had a significant and at least moderately strong univariate association with all-cause mortality, cardiac death, and arrhythmic death. Power in the lower-frequency bands--ultra low frequency (ULF) and very low frequency (VLF) power--had stronger associations with all three mortality end points than power in the higher-frequency bands--low frequency (LF) and high frequency (HF) power. The 24-hour total power also had a significant and strong association with all three mortality end points. VLF power was the only variable that was more strongly associated with arrhythmic death than with cardiac death or all-cause mortality. In multivariate Cox regression models using a step-up approach to evaluate the independent associations between frequency domain measures of heart period variability and death of all causes, ULF power was selected first (i.e., was the single component with the strongest association). Adding VLF or LF power to the Cox regression model significantly improved the prediction of outcome. With both ULF and VLF power in the Cox regression model, the addition of the other two components, LF and HF power, singly or together, did not significantly improve the prediction of all-cause mortality. We explored the relation between the heart period variability measures and all-cause mortality, cardiac death, and arrhythmic death before and after adjusting for five previously established postinfarction risk predictors: age, New York Heart Association functional class, rales in the coronary care unit, left ventricular ejection fraction, and ventricular arrhythmias detected in a 24-hour Holter ECG recording. CONCLUSIONS: After adjustment for the five risk predictors, the association between mortality and total, ULF, and VLF power remained significant and strong, whereas LF and HF power were only moderately strongly associated with mortality. The tendency for VLF power to be more strongly associated with arrhythmic death than with all-cause or cardiac death was still evident after adjusting for the five covariates. Adding measures of HPV to previously known predictors of risk after myocardial infarction identifies small subgroups with a 2.5-year mortality risk of approximately 50%.

Aged↗
PubMed1992

Time domain measurements of heart rate variability.

Assessment of HRV through time domain variables is a simple and practical method of assessing autonomic function. In this capacity its utility has been demonstrated in normal subjects and in diverse cardiac and noncardiac pathologic states. It can be used to assess the effects of drugs and other interventions, including exercise and psychological and physical stress on cardiac autonomic tone. Importantly, decreased HRV is almost uniformly associated with adverse outcome. The prognostic information appears to incorporate both alterations in autonomic tone and longer term components and is best assessed using ambulatory ECG recordings. Defining the clinical applicability and physiologic mechanisms of changes in HRV remain active areas of research.

Electrocardiography, Ambulatory↗
PubMed1991

Stability over time of variables measuring heart rate variability in normal subjects.

Both time and frequency domain measures of heart rate (HR) variability have been used to assess autonomic tone in a variety of clinical conditions. Few studies in normal subjects have been performed to determine the stability of HR variability over time, or the correlation between and within time and frequency domain measures of HR variability. Fourteen normal subjects aged 20 to 55 years were studied with baseline and placebo 24-hour ambulatory electrocardiograms performed 3 to 65 days apart to assess the reproducibility of the following time domain measures of cycle length variability: the standard deviation of all normal cycle intervals; mean normal cycle interval; mean day normal cycle interval; night/day difference in mean normal cycle interval; root-mean-square successive cycle interval difference; percentage of differences between adjacent normal cycle length intervals that are greater than 50 ms computed over the entire 24-hour electrocardiographic recording (proportion of adjacent intervals greater than 50 ms); and the frequency domain measures of high (0.15 to 40 Hz), low (0.003 to 0.15) and total (0.003 to 0.40) power. The mean and standard deviations of these measures were virtually identical between placebo and baseline measurements and within the studied time range. Variables strongly dependent on vagal tone (high-frequency, low-frequency and total power, root-mean-square successive difference, and percentage of differences between adjacent normal cycle intervals greater than 50 ms computed over the entire 24-hour electrocardiographic recording) were highly correlated (r greater than 0.8). It is concluded that measures of HR variability are stable over short periods of time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Electrocardiographic subset analysis of diltiazem administration on long-term outcome after acute myocardial infarction. The Multicenter Diltiazem Post-Infarction Trial Research Group.

The effect of diltiazem on long-term outcome after acute myocardial infarction (AMI) was assessed in 2,377 patients enrolled in the Multicenter Diltiazem Post-Infarction Trial and subsequently followed for 25 +/- 8 months. The study population included 855 patients (36%) with at least 1 prior AMI before the index infarction and 1,522 patients (64%) with a first AMI, of whom 409 (27%) had a first non-Q-wave AMI, 664 (44%) a first inferior Q-wave AMI, and 449 (30%) a first anterior Q-wave AMI. This post hoc analysis revealed that, among patients with first non-Q-wave and first inferior Q-wave AMI, there were fewer cardiac events during follow-up in the diltiazem than in the placebo group, and that the reverse was true for patients with first anterior Q-wave AMI or prior infarction. The diltiazem:placebo Cox hazard ratio (95% confidence limits) for the trial primary end point (cardiac death or nonfatal reinfarction, whichever occurred first) was: first non-Q-wave AMI-0.48 (0.26, 0.89); first inferior Q-wave AMI-0.66 (0.40, 1.09); first anterior Q-wave AMI-0.82 (0.51, 1.31); and prior AMI-1.11 (0.85, 1.44). Use of cardiac death alone as an end point gave an even more sharply focused treatment difference: first non-Q-wave AMI-0.46 (0.18, 1.21); first inferior Q-wave AMI-0.53 (0.27, 1.06); first anterior Q-wave AMI-1.28 (0.68, 2.40); prior infarction-1.26 (0.90, 1.77). Further analysis revealed that these differences in the effect of diltiazem in large part reflected the different status of the 4 electrocardiographically defined subsets in terms of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Diltiazem↗
PubMed1991

Effect of atenolol and diltiazem on heart period variability in normal persons.

Several time and frequency domain measures of heart period variability are reduced 1 to 2 weeks after myocardial infarction, and a reduced standard deviation of normal RR intervals over a 24 h period (SDNN) is associated with increased mortality. The predictive accuracy of heart period variability may be reduced by drugs used to treat patients after myocardial infarction. Accordingly, a randomized, three period, placebo-controlled, crossover (Latin square) design was used to determine the effect of atenolol and diltiazem on time and frequency measures of heart period variability calculated from 24 h continuous electrocardiographic recordings during treatment with atenolol, diltiazem and placebo in 18 normal volunteers. During atenolol treatment, the 24 h average normal RR (NN) interval increased 24% (p less than 0.001). The three measures of tonic vagal activity were significantly increased (p less than 0.001) during atenolol treatment: percent of successive normal RR intervals greater than 50 ms = 69%, root mean square successive difference of normal RR intervals = 61% and high frequency power in the heart period power spectrum = 84%. Low frequency power also increased 45% (p less than 0.01), indicating that this variable also is an indicator of tonic vagal activity over 24 h. Diltiazem had no significant effect on the 24 h average NN interval or on any measure of heart period variability. The decreased mortality rate after myocardial infarction associated with beta-adrenergic blocker but not calcium channel blocker therapy may be attributed in part to an increase in vagal tone caused by beta-blockers.

Adult↗
PubMed1990

Effect of diltiazem on cardiac rate and rhythm after myocardial infarction. Multicenter Diltiazem Postinfarction Trial Investigators.

The a priori hypothesis that diltiazem would reduce the frequency and repetitiveness of ventricular arrhythmias was tested 3 months after myocardial infarction in patients participating in the Multicenter Diltiazem Postinfarction Trial. After 3 months of follow-up, 1,546 of the 2,466 patients enrolled had a 24-hour continuous electrocardiographic recording that contained greater than or equal to 12 hours of analyzable data. They were similar to the patients who survived 3 months but chose not to have a 24-hour electrocardiographic recording (i.e., they were representative of the entire group that survived 3 months). After 3 months of follow-up, there were no significant differences between the diltiazem and placebo groups in the prevalence of atrioventricular block, the frequency of atrial arrhythmias or the frequency or repetitiveness of ventricular arrhythmias. Heart rate was significantly lower (67 +/- 12 vs 71 +/- 12 beats/min) and there was a significantly greater proportion of patients with sinus pauses greater than or equal to 2 seconds in duration in the diltiazem group (6%) than in the placebo group (3%). Comparison with placebo revealed no evidence either for an anti- or proarrhythmic effect of diltiazem. There was no reduction in sudden or arrhythmic death attributable to diltiazem treatment; the fraction of total deaths that were arrhythmic by the Hinkle classification was 41% in the placebo group and 42% in the diltiazem group. It may be that the lack of effect of diltiazem on ventricular arrhythmias is partially responsible for its lack of effect on mortality after myocardial infarction.

Adult↗
PubMed1990

The independence of cycle length variability and exercise testing on predicting mortality of patients surviving acute myocardial infarction. The Multicenter Postinfarction Research Group.

Cycle length variability (CLV), defined as the standard deviation of normal cycle length intervals, has been found to be a powerful predictor of subsequent mortality in a population of 808 survivors of acute myocardial infarction. Decreased CLV is associated with a significant increase in mortality. CLV remained an independent predictor of outcome even after adjusting for left ventricular ejection fraction, clinical risk factors, heart rate and ventricular arrhythmias. In the same population of survivors of acute myocardial infarction, the results of exercise testing also strongly predicted outcome, with those failing to take the test having the worst survival, and those completing the low-level stress test taken before discharge having the best prognosis. The hypothesis that the status of stress test (completed; did not complete; failed to take) and CLV were measuring the same factor related to mortality was tested. Although the distribution of CLV was shifted to higher CLV in patients who completed the test and to lower CLV in those who failed to take the test, both predictors of mortality remained independent predictors of long-term mortality (average of 31 months of follow-up) after controlling for each other. Moreover, subgroups with an approximate 15-fold difference in mortality were defined using both variables (CLV less than 50 ms, did not take test had a 54% mortality; CLV greater than 100 ms, completed the test had a mortality of 3.5%). CLV is a measure of autonomic tone; it is not strongly related to exercise ability and using the results of both stress testing and CLV results in the identification of subgroups of postinfarction patients with markedly disparate risks of mortality.

Blood Pressure↗
PubMed1990

Frequency and significance of late evolution of Q waves in patients with initial non-Q-wave acute myocardial infarction. Diltiazem Reinfarction Study Group.

Serial 12-lead electrocardiogram and plasma creatine kinase (CK)-MB values from 544 patients with confirmed non-Q-wave acute myocardial infarction (AMI) were analyzed to define the rate of progression of non-Q-wave AMI to Q-wave AMI and to examine its relation to CK-MB evidence of extension. The baseline electrocardiogram was obtained 50 +/- 10 hours after AMI and compared with subsequent electrocardiograms at 48 and 72 hours after baseline record and at discharge. Plasma CK-MB was assayed every 12 hours after baseline. A total of 76 patients (14%) progressed to Q-wave AMI. Compared to the 468 patients who retained non-Q-wave AMI, those patients who evolved Q-wave AMI were more likely to exhibit ST elevation greater than or equal to 1.0 mm in greater than or equal to 2 infarct-related leads (49 vs 32%, p less than 0.005), higher peak CK values with the index AMI (754 +/- 625 vs 611 +/- 604 IU; p = 0.0018) and a greater incidence of CK-MB-confirmed extensions (18.5 vs 5.5%, p less than 0.0001). For those patients progressing to Q-wave AMI within 48 hours of baseline electrocardiogram, CK-MB extension occurred in 9.5% (4 of 42) versus 29.4% (10 of 34) of those who progressed after 48 hours (p = 0.0262). A distinct minority (14%) of patients with non-Q-wave AMI will develop Q waves before discharge. The progression to Q-wave AMI after initial non-Q-wave AMI appears to involve 2 different mechanisms: temporal lag in the electrocardiogram, and actual extension by quantitative CK-MB criteria.

Creatine Kinase↗
PubMed1990

Differential risk patterns associated with 3 month as compared with 3 to 12 month mortality and reinfarction after non-Q wave myocardial infarction. The Diltiazem Reinfarction Study Group.

Follow-up data for 515 survivors of acute non-Q wave myocardial infarction were categorized according to mortality: 1) between hospital discharge and 3 months after infarction (early), and 2) between 3 and 12 months after infarction (late). The mortality rate decreased steadily for the first 3 months and was constant thereafter. There were 25 early and 32 late deaths. After adjustment for the longer time associated with the 3 to 12 month period, the relative risk per unit time of early as compared with late mortality was 2.64. Risk factors for early mortality were different from those that predicted late mortality. Independent predictors of mortality between hospital discharge to 3 months after infarction were ST segment depression that persisted during hospitalization (p less than 0.0001), in-hospital reinfarction (p = 0.0006) and a history of congestive heart failure (p = 0.0255). Persistent ST depression and in-hospital reinfarction had neither a univariate nor an independent association with 3 to 12 month mortality. Age (p less than 0.0001), reinfarction between discharge and 3 months (p = 0.0147) and diabetes (p = 0.0404) were independently associated with late mortality. Early mortality was only 0.5% (1 of 199) in patients with no ST depression at either baseline or discharge (group 1); 4.8% (8 of 168) in those with ST depression at exactly one time point (group 2) and 13.7% (16 of 117) in those who had ST depression present at both time points (group 3). All pairwise differences were significant (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Double-Blind Method↗
PubMed1989

Efficacy and safety of intravenous diltiazem for treatment of atrial fibrillation and atrial flutter. The Diltiazem-Atrial Fibrillation/Flutter Study Group.

This study evaluates the effectiveness and safety of intravenous diltiazem for the treatment of atrial fibrillation and atrial flutter. A double-blind, parallel, randomized, placebo-controlled protocol was used, and 6 large, urban hospitals, both university-affiliated and private, participated. The study involved 113 patients with atrial fibrillation or flutter, a ventricular rate greater than or equal to 120 beats/min and systolic blood pressure greater than or equal to 90 mm Hg without severe heart failure. The dose of intravenous diltiazem (or identical placebo) was 0.25 mg/kg/2 minutes followed 15 minutes later by 0.35 mg/kg/2 minutes if the first dose was tolerated but ineffective. If a patient did not respond, the code was broken and the patient was allowed to receive open-label diltiazem if placebo had been given. Of 56 patients, 42 (75%) randomized to receive diltiazem responded to 0.25 mg/kg and 10 of 14 responded to 0.35 mg/kg, for a total response rate of 52 of 56 patients (93%), whereas 7 of 57 patients (12%) responded to placebo (p less than 0.001). After the double-blind protocol, 49 of the 57 patients who received placebo were then given diltiazem; 47 of 49 responded, for an overall response rate of 99 of 105 patients (94%) with diltiazem. The median time from the start of drug infusion to the maximal decrease in heart rate was 4.3 minutes. Side effects occurred in 14 patients, 7 of whom had asymptomatic hypotension not requiring intervention. Thus, intravenous diltiazem was rapidly effective for slowing the ventricular response in most patients with atrial fibrillation or atrial flutter. Blood pressure decreased slightly. Side effects were mild.

Aged↗
PubMed1989

Favourable long term prognosis in patients with non-Q wave acute myocardial infarction not associated with specific electrocardiographic changes. Diltiazem Reinfarction Study Research Group.

Electrocardiograms obtained serially from 544 patients with non-Q wave infarction in the Diltiazem Reinfarction Study were analysed to compare the short term (less than or equal to 14 days) and long term (one year) follow up of 105 patients (19%) whose admission electrocardiogram showed no localisable repolarisation abnormalities (group 1) with the outcome in 439 patients (81%) who had ST-T wave abnormalities (group 2) localised to two or more contiguous leads within an anterior, inferior, or lateral lead group. There were no major between group differences in baseline clinical variables, concomitant medications, or treatment allocation (diltiazem v placebo). Group 2 patients, in the first year, had a higher incidence of early recurrent ischaemia (angina greater than or equal to 24 hours after myocardial infarction associated with ischaemic repolarisation changes), reinfarction, and readmission for chest pain than group 1 patients, despite comparable creatine kinase and creatine kinase MB activities in both groups. About 20% of patients with acute non-Q wave myocardial infarction did not have definable ST-T wave abnormalities. These patients had a similar clinical and enzymatic profile as patients with non-Q wave infarction with definable ST-T wave abnormalities and they were more likely to have a favourable short term and long term outcome.

Creatine Kinase↗
PubMed1989

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction.

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.

Creatine Kinase↗
PubMed1989

Risk stratification of patients with non-Q wave myocardial infarction. The critical role of ST segment depression. The Diltiazem Reinfarction Study Research Group.

One-year follow-up data on 515 patients who survived hospitalization with MB-creatine kinase-confirmed, acute non-Q wave myocardial infarction were analyzed for factors related to mortality (n = 57) and late reinfarction (n = 64). Twelve of 24 analyzed variables were significantly associated with mortality. Those factors, which were independently predictive of mortality by Cox regression analysis, were persistent ST depression (p = 0.0009), a history of congestive heart failure (CHF) (p = 0.0069), older age (p = 0.0128), and ST elevation at hospital discharge (p = 0.0173). In-hospital reinfarction achieved borderline significance (p = 0.0512). Mortality during the follow-up period was 5.5% in patients with no ST depression, 10.1% in those with ST depression at baseline or discharge, and 22.2% in patients with ST depression at baseline and discharge (i.e., "persistent" ST depression). The age-adjusted risk of mortality for patients with persistent ST depression, discharge-ST elevation, and CHF was 13.99 times as high as was the risk for patients with no ST depression, no discharge-ST elevation, and no CHF. Of the 483 patients with complete electrocardiographic data at both baseline and discharge, 203 (42%) could be stratified into a high risk population with a risk ratio for 1-year mortality more than sevenfold that of patients with no risk factors. Although persistent ST depression was significantly associated with several measures of structural left ventricular damage, the independent significance of ST depression persisted even after adjusting for these factors. The independent predictors of late reinfarction (persistent ST depression, p = 0.0058; Killip class II or III, p = 0.0106; and left ventricular hypertrophy, p = 0.0470) permitted a similar risk stratification. We conclude that 1) easily identified clinical and electrocardiographic factors permit stratification of patients with non-Q wave infarction into high-risk subsets who may benefit from aggressive therapy; 2) ST depression is a highly significant and independent predictor of poor prognosis; and 3) the powerful predictive value of persistent ST depression suggests that non-Q wave myocardial infarction patients with this depression should be viewed as potentially high-risk patients who may be candidates for additional noninvasive testing or early coronary angiography.

Diltiazem↗
PubMed1988

Clinical significance and prognostic importance of left ventricular hypertrophy in non-Q-wave acute myocardial infarction.

Left ventricular (LV) hypertrophy is known to be an independent risk factor for cardiac death, but its significance in non-Q-wave acute myocardial infarction (AMI) has not been assessed previously. In a randomized diltiazem-placebo-controlled therapeutic trial of non-Q-wave AMI confirmed by creatine kinase-MB (CK-MB), 126 of 544 patients (23%) exhibited LV hypertrophy using standard voltage criteria. Compared to patients without LV hypertrophy, patients with LV hypertrophy were significantly older (65 vs 60 years, p less than 0.0001) and had smaller peak adjusted CK levels (490 +/- 376 vs 666 +/- 726 IU/liter, p less than 0.001) than patients without LV hypertrophy. Patients with and without LV hypertrophy did not differ significantly in acute mortality during hospitalization, progression to Q waves, reinfarction by CK-MB criteria or angina associated with transient electrocardiographic changes. Compared with patients without LV hypertrophy, those patients with non-Q-wave AMI and LV hypertrophy had a 2-fold higher incidence of reinfarction (24 vs 12%, p less than 0.005) and death (19 vs 9%, p = 0.044) during the first year of follow-up. Multivariate regression analysis revealed that the relative risk of death and reinfarction during the initial year after AMI was increased by a factor of 1.7 and 2.1 among patients with LV hypertrophy, respectively. It was therefore concluded that, although patients with LV hypertrophy and non-Q-wave AMI have smaller enzymatic infarcts and the same short-term prognosis as do patients without LV hypertrophy, their reinfarction and mortality rates are significantly increased during the first year of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1988

Correlation of heart rate variability with clinical and angiographic variables and late mortality after coronary angiography.

Decreased heart rate (HR) variability is associated with increased mortality after myocardial infarction, but the prognostic value of HR variability in patients without recent myocardial infarction and its correlation with other clinical and angiographic data have not previously been reported. In the present study, detailed clinical assessments and 24-hour ambulatory electrocardiograms were performed prospectively on 100 patients undergoing elective coronary angiography. HR variability was inversely correlated with HR (r = -0.38, p = 0.001), diabetes mellitus (r = -0.22, p = 0.025) and digoxin use (r = -0.29, p = 0.004), but not with left ventricular ejection fraction, extent of coronary artery disease or other clinical, electrocardiographic or angiographic variables. All patients were followed for 1 year. Major clinical events after initial discharge occurred in 10 patients and included 6 deaths and 4 coronary bypass operations. Left ventricular ejection fraction was the only variable that correlated with the occurrence of a clinical event (p = 0.002). Decreased HR variability and ejection fraction were the best predictors of mortality (both p less than 0.01), and the contribution of HR variability to mortality was independent of ejection fraction, extent of coronary artery disease and other variables. Furthermore, 11 patients with HR variability less than 50 ms had an 18-fold increase in mortality compared with patients with HR variability greater than 50 ms (36 vs 2%, p = 0.001). Thus, decreased HR variability is a potent independent predictor of mortality in the 12 months following elective coronary angiography in patients without recent myocardial infarction.

Adult↗