Is abnormal heart rate variability a specific feature of congestive heart failure?
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Biomedical subjects
Publications and source records attributed to S Chakko.
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Cor-triatriatum is an uncommon congenital cardiac anomaly. In this case report, transesophageal echocardiographic and operative findings in a 57-year-old female with cor-triatriatum are presented.
This study revealed that conventional temporal and spectral indexes of heart rate variability were reduced in patients with sinus tachycardia due to various, easily detectable, causes. These findings were attributed to the fast rates, per se, regardless of the cause, without reflecting a particular shift in the degree of autonomic activity and tone.
The presence of late potentials (LPs) on signal-averaged electrocardiography (SAECG) is predictive of ventricular tachycardia. The effect of hemodialysis (HD) on SAECG has not been well studied. SAECG was evaluated in 28 patients with chronic renal failure immediately before and after HD. In each SAECG, QRS duration, low-amplitude signal duration (LASd), and root-mean-square voltage of the terminal 40 milliseconds of the QRS (RMS40) were measured. To evaluate the effect of fluid removal on SAECG, the last 12 patients were studied during two different HD sessions, one with and one without fluid removal. Two-dimensional echocardiography was performed before and after HD on these 12 patients. At baseline, four patients met the criteria for LPs on SAECG. Only one patient met the criteria for LPs on SAECG after HD. After HD, the mean LASd decreased (28.3 +/- 12.9 to 24.9 +/- 10.1 milliseconds; P = 0.041) and RMS40 increased (63.0 +/- 56.9 to 79.0 +/- 59.2 microV; P = 0. 006). Among the 12 patients who underwent HD with and without fluid removal, left ventricular end-diastolic dimension decreased with (5. 4 +/- 0.6 to 5.1 +/- 0.6 cm; P = 0.024) but not without fluid removal (5.2 +/- 0.3 to 5.1 +/- 0.4 cm; P = not significant [NS]). RMS40 improved with (43.8 +/- 23.1 to 53.2 +/- 22.6 microV; P = 0. 03) but not without fluid removal (51.0 +/- 26.5 to 51.5 +/- 24.2 microV; P = NS). A significant negative correlation was found between change in body weight and change in RMS40 parameter (r = 0. 456; P = 0.0381). SAECG parameters are abnormal in a significant proportion of patients with chronic renal failure and improve with HD despite electrolyte and other proarrhythmic changes. Decreased left ventricular dimension because of fluid removal during HD is one possible explanation for this improvement.
Analysis of heart rate variability in patients with inappropriate sinus tachycardia showed a 24-hour decrease in all temporal and spectral indexes, even after attempted correction to a rate of 75 beats/min. This may have resulted from a global decrease in parasympathetic activity or from a rapid sinus rate produced by other ill-defined mechanisms.
In patients with congestive heart failure, abnormal heart rate variability is a predictor of total mortality and sudden cardiac death. Drugs that improve heart rate variability may have a potential role for improving the survival among these patients. The effects of clonidine were studied in 24 patients with congestive heart failure, sinus rhythm, a left ventricular ejection fraction <0.40, and systolic blood pressure > 115 mm Hg. A 6-minute corridor walk test and 24-hour Holter monitoring were performed before and 42+/-24 days after initiation of clonidine therapy (Catapres-TTS patch, mean dose: 0.33+/-0.21 mg). Changes in other medications used at baseline were not allowed. One patient died suddenly. Two patients did not complete the protocol due to worsening congestive heart failure, which required changes in medications, 1 patient discontinued due to hypotension, and 2 for personal reasons. Among the 18 patients who completed the protocol, the mean RR interval of sinus beats increased from 760+/-106 to 822+/-125 ms (p=0.001) and the distance covered during the 6-minute walk test increased from 1,148+/-277 to 1,255+/-359 feet (p=0.042). Systolic blood pressure decreased from 139+/-15 to 119+/-10 mm Hg (p <0.0001). The following increases were noted in the heart rate variability measurements: high-frequency power in 0.15 to 0.40 Hz: 4.58+/-1.07 to 4.94+/-1.17 In (ms), p=0.002; SD: 47.0+/-16.9 to 52.5+/-18.4 ms, p=0.034; SD of the mean of all RR intervals in 24 hours: 116+/-94 to 130+/-19 ms, p=0.033; SD of all 5-minute mean RR intervals: 106+/-44 to 124+/-66 ms, p=0.042; root-mean square of difference of successive RR intervals: 28.8+/-10.7 to 34.1+/-14.2 ms, p=0.017. Clonidine improves heart rate variability in the patients with congestive heart failure by increasing the parasympathetic tone. It is well tolerated by most patients with heart failure and may have a beneficial effect on exercise capacity.
The usefulness and cost of echocardiography was evaluated in 133 consecutive patients admitted to the Coronary Care Unit. A useful echocardiogram was one that provided new information, which influenced diagnosis, prognosis, or treatment. The cost of a useful echocardiogram was defined as the unit cost ($476 the Medicare global fee) x units (i.e., total echocardiograms / useful echocardiograms). Admission diagnoses were unstable angina (34%), arrhythmia (14%), congestive heart failure (8%), postprocedure monitoring (7%), acute myocardial infarction (6%), and miscellaneous (20%). The echocardiogram provided new information in 29% of patients. Patients without a recent echocardiogram (within 3 months) were twice as likely to have a useful echocardiogram (33 of 99, 33%) as those with a recent echocardiogram (5 of 34, 15%, p <0.05). A cardiologist predicted the overall usefulness of echocardiography with a positive predictive accuracy of 52% and a negative predictive accuracy of 94% (p < 0.0001). The overall cost of a useful echocardiogram of 3.5 units or $1,666 per useful study was decreased to $904 (1.9 units) if only studies predicted to be useful were considered. The usefulness of echocardiography varied significantly (p <0.02) within the admitting diagnostic categories. The usefulness of an echocardiogram was underestimated in patients with congestive heart failure, where it was found to be most useful (64%; $762 or 1.6 units). Thus, usefulness relates to the admission diagnosis, the availability of a recent echocardiogram, and to clinical judgment.
Diastolic Doppler filling parameters were measured before and after hemodialyses, performed once with and once without fluid removal. Changes occurred only with fluid removal and correlated with weight loss, indicating that they are the result of reduction in preload.
Clinical and experimental studies demonstrate that calcium (Ca2+) overload in myocardial cells is an important factor in the genesis of various serious arrhythmias. Calcium antagonists block voltage-dependent channels and thus reduce entry of Ca2+ into heart cells. Because of their specificity for atrioventricular nodal cells, verapamil and diltiazem are used clinically to treat supraventricular arrhythmias involving transmission in the atrioventricular node. These two drugs and the dihydropyridine (DHP) calcium antagonists have been shown to prevent ventricular ischemic and reperfusion arrhythmias in the laboratory. Despite these data indicating that calcium antagonists are antiarrhythmic, a recent controversy has raised the possibility that certain calcium antagonists are unsafe to use, especially for patients with coronary heart disease. Proarrhythmia has been proposed to be a mechanism contributing to potentially adverse outcomes. Although excessive concentrations of verapamil and diltiazem may cause sino-atrial nodal asystole and varying degrees of atrioventricular block, there is little direct evidence that this contributes to significant proarrhythmia, for example, ventricular tachyarrhythmias. Nonetheless, although it appears paradoxical that agents which block the entry of Ca2+ into heart cells may be considered arrhythmogenic, there are circumstances under which dosage with certain calcium antagonists potentially leads to myocardial Ca2+ overload. For example, bouts of neurohormonal activation brought about by calcium antagonist-induced abrupt reductions in blood pressure may be accompanied each time by significant beta-adrenergic-enhanced influx of Ca2+ through the L-type cardiac calcium channels. This elevates the intracellular Ca2+ concentration and disturbs Ca2+ regulation, especially in diseased hearts whose intracellular Ca2+ regulation has already been compromised, and might induce alterations in cardiac electrical activity. In the present article, interactions among cardiac calcium channels, classes of calcium antagonists, and specific formulations of certain antagonists are considered with respect to directly induced ventricular arrhythmogenesis. Indirect potentially proarrhythmic actions of the calcium antagonists are also discussed. We outline some of the many questions that remain to be answered with respect to the actions of DHP on the heart including that of whether beta-adrenergic stimulation modifies the degree of cardiac Ca2+ channel inhibition by DHP-type calcium antagonists.
Heart rate variability (HRV) was evaluated during the first 24 hours of hospitalization in 36 patients with acute myocardial infarction. Reperfusion was achieved by 60 minutes in 21 patients (group M1) and by 130 minutes in the remaining 15 (group M2). Mean 24-hour HRV measures were not significantly different between groups M1 and M2. Hourly spectral analysis revealed a decrease in total power (0.01 to 1.0 Hz) from 0 to 8 hours to 9 to 16 and 17 to 24 hours in groups M1 (7.04 +/- 0.27 to 6.94 +/- 0.28 and 6.52 +/- 0.18; p = 0.0006) and in group M2 (6.88 +/- 0.30 to 6.57 +/- 0.23 and 6.40 +/- 0.15; p = 0.002). Total power decreased immediately after reperfusion: in group M1 it decreased during the second hour (7.32 +/- 0.96 to 6.42 +/- 1.2; p = 0.001) and in group M2 during the third (7.47 +/- 1.2 to 6.73 +/- 1.4; p = 0.049) and fourth hours (7.47 +/- 1.2 to 6.48 +/- 1.4; p = 0.029). Mean change in total power in the second hour was -11.6% in group M1 and +3.9% in group M2 (p = 0.0001) and in the third hour, +14.5% in group M1 and -8.6% in group M2 (p = 0.006). During the remaining 21 hours, there was no significant difference in hourly change in total power between groups. Similar changes were noted in high-frequency power, but the ratio of low-frequency to high-frequency power was unchanged. In acute myocardial infarction, HRV is higher during the early phase and decreases as hours progress. Reperfusion causes an immediate, transient, and seemingly paradoxic decrease in HRV, probably because of an abrupt decrease in parasympathetic tone.
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Cardiac complications of cocaine abuse and a rational approach to evaluating and managing them are described. Cardiac abnormalities reported among asymptomatic cocaine abusers include echocardiographic left ventricular hypertrophy and segmental wall motion abnormalities. Electrocardiogram may reveal increased QRS voltage, ST-T changes, and pathologic Q waves. Episodes of ST elevation may be seen during Holter monitoring. The management of cocaine-abusing patients who present to an emergency room with acute chest pain is controversial because the two reported studies yielded conflicting results regarding the incidence of myocardial infarction (MI). Even in the absence of infarction, electrocardiographic abnormalities are common among these patients, which complicates the decision-making regarding hospitalization. Pathophysiology of cocaine-related MI is discussed. Distinct clinical features of cocaine-related MI make it clear that the association between the two is not just temporal. However, considering the number of persons abusing cocaine, it is a rarity. Beta-adrenergic blockers should be avoided in the treatment of cocaine-induced myocardial ischemia which is best treated with nitrates and calcium-channel blockers. Reports of cocaine-induced myocarditis and cardiomyopathy are reviewed. Experimental studies and clinical case reports suggest that cocaine may cause lethal arrhythmias. Cocaine prolongs repolarization by a depressant effect on potassium current and may generate early afterdepolarizations. It is possible that cocaine-associated arrhythmias are secondary to vasospasm-related ischemia and reperfusion as well.
OBJECTIVES: This study was designed to test the hypothesis that monitoring the ST segment on a single electrocardiographic (ECG) lead reflecting activity in the infarct zone provides sensitive and specific recognition of reperfusion within 60 min of initiation of therapy in acute myocardial infarction. BACKGROUND: Infarct-related arteries that fail to recanalize early may benefit from immediate rescue angioplasty. Hence, detection of reperfusion has important practical clinical implications. METHODS: Of 41 patients with acute myocardial infarction who had ambulatory ECG (Holter) monitors placed, 38 had adequate ST segment monitoring for 3 h; 35 of the 38 were treated with thrombolytic agents and 3 with primary angioplasty. All patients underwent early coronary angiography and were classified into two groups: Group P (22 patients) had angiographic patency (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow), the Group O (16 patients) had persistent occlusion (TIMI grade 0 or 1 flow) of the infarct-related vessel at 60 min from initiation of therapy. The initial ST segment level was defined as the first ST segment level recorded; the peak ST segment level was defined as the highest ST segment level measured during the 1st 60 min. To assess the optimal ST segment recovery criteria for reperfusion, the presence or absence of a > or = 75%, > or = 50% and > or = 25% decrement from initial and peak ST segment levels, sampled and analyzed at 2.5-, 5-, 10-, 15-and 20-min intervals, was correlated with patency of the infarct-related artery at 60 min. RESULTS: ST segment recovery of > or = 50% reduction from peak ST segment levels with sampling rates at < or = 10-min intervals provided the optimal criterion for recognizing coronary artery patency at 60 min (sensitivity 96%, 95% confidence interval [CI] 77% to 99%; specificity 94%, 95% CI 69% to 99%, p < 0.0001). The subgroup of 13 patients in Group P with TIMI grade 3 reperfusion flow all met this criterion (sensitivity 100%, 95% CI 75% to 100%). The use of the initial ST segment level as the baseline for determining the presence of a > or = 50% reduction in ST segment levels within 60 min was less sensitive. Prediction of coronary reperfusion within 60 min of therapy on the basis of a > or = 75% decrement from peak ST segment levels was less sensitive, and the use of a > or = 25% decrement was less specific. CONCLUSIONS: ST segment monitoring of a single lead reflecting the infarct zone provides a reliable method for assessing reperfusion within 60 min of acute myocardial infarction. Optimal criteria for ECG reperfusion include a > or = 50% decrease from peak ST segment levels, with ST segment measurements recorded continuously or at least every 10 min.
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Electrocardiographic abnormalities of 200 asymptomatic, chronic cocaine abusers (aged < or = 45 years, 69% black) admitted for rehabilitation (group 1) were compared with 38 cocaine abusers treated in the emergency room (group 2), 21 cocaine abusers who died suddenly (group 3), and 425 control subjects from the general population. In group 1, 39% of electrocardiograms were abnormal: Increased QRS voltage was noted in 27%, ST elevation in 22%, ST-T changes in 17%, and prior myocardial infarction in 3%. Increased QRS voltage (35% vs 10%, p = 0.00007) and ST elevation (26% vs 13%, p = 0.0278) were more prevalent in blacks than in whites. With use of Minnesota coding, electrocardiograms in group 1 were compared with those of 141 black and 284 white men (aged < 40 years) from the general population. ST elevation was more prevalent in both black (22% vs 8%, p = 0.00073) and white (15% vs 1%, p < 0.00001) cocaine abusers than in the general population. Compared with group 1, group 2 had higher prevalence of sinus tachycardia (16% vs 1%, p = 0.0002), supraventricular tachycardia (5% vs 0%, p = 0.024), ST-T changes (34% vs 17%, p = 0.0164), and QTc > 440 ms (26% vs 4%, p = 0.00003); mean QTc was also greater among group 2 subjects (427 +/- 38 vs 404 +/- 19 ms, p < 0.0001). In group 3, QTc was > 440 ms in 6 of 8 subjects (75%) with 12-lead electrocardiograms.(ABSTRACT TRUNCATED AT 250 WORDS)