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K M Kessler

Publications and source records attributed to K M Kessler.

At least 55 records · Page 3Linked to original sources
PubMed1995

Acute myocardial infarction. Then and now.

Dramatic changes in the management of acute myocardial infarction (AMI) have occurred in the past decade. While previous management strategies were primarily supportive, current strategies focus on achieving and maintaining patency of the infarct-related artery restoring blood flow to jeopardized myocytes, preserving left ventricular function, and preventing recurrences and complications in addition to promoting healing. Restoration of blood flow can be achieved pharmacologically with thrombolytic agents or mechanically with percutaneous transluminal coronary angioplasty (PTCA). Early use of antiplatelet agents and anticoagulants helps maintain patency of the infarct-related arteries and prevents thromboembolic complications. Administration of beta-blockers and angiotensin enzyme inhibitors are more specific means of conserving myocardium and preserving ventricular function. Additionally, several strategies for preventing arrhythmias such as prophylactic lidocaine use and routine long-term suppression of premature ventricular contractions with antiarrhythmic drugs are no longer routinely advocated. Basically, in the era prior to the eighth decade of this century, the primary direction of the therapeutic strategy for AMI was to reduce the oxygen demands in the infarcted myocardium; whereas in the subsequent years, the emphasis shifts to improvement in oxygen delivery, via thrombolysis, PTCA, and coronary artery bypass graft surgery. These interventional changes, when added to greater sophistication in the use of drugs to reduce oxygen demands, resulted in significant lowering of myocardial mortality.

Aged↗
PubMed1994

Frequency and type of electrocardiographic abnormalities in cocaine abusers (electrocardiogram in cocaine abuse).

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)

Adult↗
PubMed1994

Future evaluation of antiarrhythmic therapy.

The expansion of antiarrhythmic therapy beyond pharmacologic agents to include surgery, devices, and ablation procedures, plus the reaffirmation by the Cardiac Arrhythmia Suppression Trial (CAST) of the need for concurrent placebo-controlled trials to establish a mortality benefit, have resulted in the need to consider the requirements for evaluating therapy. Pharmacologic therapy may be used in three ways: (1) primary; (2) alternative; and (3) adjunctive. To accurately identify a mortality benefit from primary therapy, a placebo-controlled study is necessary. In contrast, control of symptoms may be identified without the same rigorous demands. Current data are limited by the absence of true negative controls for most interventions that claim a possible mortality benefit. Alternative therapy provides a choice between equally effective therapies, neither of which has necessarily been documented to have a mortality benefit. Adjunctive therapy is that which is used for control of symptoms, whereas another therapy is used to provide a presumed or proved mortality benefit. For any of these approaches, therapy must be further evaluated in terms of four modifying variables: (1) impact of therapy on the basis of both its efficacy and efficiency; (2) interpretation of outcome data based on analysis of competing risks; (3) measurement of efficacy in terms of extension of life; and (4) analysis of outcome as the equilibrium between antiarrhythmic benefit and proarrhythmic risk. With these approaches a rational analysis of the effect of therapy and its cost-based benefit can be achieved.

Anti-Arrhythmia Agents↗
PubMed1994

Cardiovascular manifestations of cocaine abuse. A case of recurrent dilated cardiomyopathy.

The medical complications of cocaine abuse are being encountered by clinicians with increasing frequency. The cardiovascular manifestations of cocaine abuse include chest pain, myocardial ischemia and infarction, congestive heart failure, arrhythmias, infective endocarditis, and aortic dissection. The pathogenesis of these cardiovascular complications has not been fully elucidated but may be related to a combination of the sympathomimetic and membrane anaesthetic effects of cocaine. We present these concepts in a case discussion format.

Arrhythmias, Cardiac↗
PubMed1993

Sudden cardiac death: epidemiology, transient risk, and intervention assessment.

PURPOSE: To integrate information from the various disciplines that contribute to the understanding of the cause and prevention of sudden cardiac death: identification of new approaches from applied clinical epidemiology; identification and control of transient risk factors; and evaluation of the results of interventions. DATA SOURCES: A broad range of research reports and interpretations of data from English-language journal articles and reviews, published primarily between 1970 and 1993. The fields of study included epidemiology, experimental electrophysiology, clinical observations, and interventions. STUDY SELECTION: Continuous literature surveys, done in relation to ongoing clinical and experimental research on sudden cardiac death since 1972. DATA EXTRACTION: Included on the basis of relevance to the topics discussed and with confirmation of data and concepts by more than one investigator when available. DATA SYNTHESIS: Information from several disciplines was integrated by the authors to synthesize new ways to view the problem of sudden cardiac death. Quantitative information was used primarily to derive qualitative statements about new perspectives on sudden cardiac death. CONCLUSIONS: Progress in the prevention of sudden death will require development of new approaches, including epidemiologic techniques to address risk characteristics specific to the problem; characterization of triggering events and identification of specific persons at risk for responding adversely to these events; and methods of evaluating outcomes appropriate to the nature of sudden cardiac death.

Cardiovascular Diseases↗
PubMed1993

Alterations in heart rate variability and its circadian rhythm in hypertensive patients with left ventricular hypertrophy free of coronary artery disease.

Heart rate variability (HRV) and its circadian rhythm were evaluated in 22 patients with treated hypertension and left ventricular hypertrophy in whom coronary artery disease was excluded by stress thallium or angiography. By using 24-hour Holter monitoring, HRV and its spectral components were measured. Findings were compared with 11 age-matched normal controls. The difference between mean R-R intervals during sleep (11 PM to 7 AM) and while awake (9 AM to 9 PM) (73 +/- 33 vs 263 +/- 63 msec, p < 0.0001) and the mean 24-hour SD of the R-R intervals (55 +/- 6.3 vs 93 +/- 11, p < 0.0001) were lower among the hypertensive patients compared with controls. The percentage of difference between successive R-R intervals that exceeded 50 msec, a measure of parasympathetic tone, was also lower among the hypertensive patients (6.8 +/- 7.1 vs 13.6 +/- 8.9, p < 0.002); it increased at night and decreased during the day among the controls, and this circadian rhythm was blunted among the patients. Spectral analysis showed that power in the high-frequency range (0.15 to 0.40 Hz) was lower among the hypertensive patients during 21 of 24 hours but that the difference was statistically significant only during 9 hours (p ranging from < 0.05 to 0.009). Power in the low-frequency range (0.04 to 015 Hz) was lower at night, increased in the morning, and higher during the day among controls; this circadian rhythm was absent among hypertensive patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Frequency domain measures of heart rate variability before the onset of nonsustained and sustained ventricular tachycardia in patients with coronary artery disease.

BACKGROUND: Low heart rate variability (HRV) is associated with an increased risk of arrhythmic death and ventricular tachycardia (VT). The purpose of this study was to examine whether there is a temporal relation between changes in HRV and the onset of spontaneous episodes of VT in patients at high risk of life-threatening arrhythmias. METHODS AND RESULTS: Components of HRV in the frequency domain were analyzed before the onset of 28 episodes of nonsustained VT (more than four impulses; duration < 30 seconds) and 12 episodes of sustained VT (> 30 seconds or requiring defibrillation) in 18 patients with coronary artery disease. Seven patients had survived cardiac arrest not associated with acute myocardial infarction, and 11 had a history of sustained VT. All frequency domain measures of HRV, i.e., total power (p < 0.001), high-frequency power (p < 0.05), low-frequency power (p < 0.01), very-low-frequency power (p < 0.01), and ultralow-frequency power (p < 0.05), were significantly lower before the onset of sustained VT than before nonsustained VT. Total power of HRV was also lower during the 1-hour period before the onset of sustained VT than the average 24-hour HRV (p < 0.05). An indirect correlation existed between the length of VT and the total power of HRV analyzed during the 15 minutes before the onset of VT (r = 0.54, p < 0.01). HRV had a trend toward increasing values before the onset of nonsustained VT (p < 0.01) but not before the sustained VT episodes. The ratio between low-frequency and high-frequency powers increased substantially before both nonsustained and sustained VT episodes (p = 0.06 and p = 0.05, respectively). The rate of VT or the coupling interval initiating the VT did not differ significantly between the nonsustained and sustained VT. CONCLUSIONS: Spontaneous episodes of VT are preceded by changes in HRV in the frequency domain. Divergent dynamics of HRV before the onset of nonsustained and sustained VT episodes may reflect differences in factors that can facilitate the perpetuation of these arrhythmias.

Aged↗
PubMed1993

Acute right ventricular infarction mimicking extensive anterolateral wall injury.

A patient presented with an acute right ventricular infarction characterized by an electrocardiographic current of injury in both the inferior (2,3,aVF) and anterior precordial leads (V1-V6). Cardiac catheterization demonstrated normal left ventricular wall motion, a codominant circulation, and severe disease of the right coronary artery. We propose that this coronary anatomy explains the injury currents on the electrocardiogram. This case illustrates a rare presentation of right ventricular myocardial infarction mimicking an extensive anterolateral wall injury.

Coronary Angiography↗
PubMed1993

Obstructive vs nonobstructive dilatation of the renal collecting system in children: distinction with duplex sonography.

OBJECTIVE: The resistive index in cortical or arcuate renal arteries of children was calculated to determine whether obstructive uropathy could be differentiated from nonobstructive dilatation. SUBJECTS AND METHODS: Kidneys (n = 176) were prospectively evaluated by using duplex Doppler sonography in patients 3 days to 20 years old. Obstruction was confirmed by renography with furosemide and/or by surgery. RESULTS: The normal resistive index was 0.57 +/- 0.06 and the normal difference in resistive indexes between kidneys was 0.03 +/- 0.02 (n = 15). Abnormal values indicative of ureteropelvic junction obstruction were defined as the normal mean +/- 2 SD (i.e., a resistive index of > or = 0.70 plus a difference in resistive indexes between kidneys of > or = 0.08). Patients with unilateral dilatation and obstruction at the ureteropelvic junction (n = 20) had a mean resistive index of 0.77 +/- 0.05 and a difference in resistive indexes between kidneys of 0.16 +/- 0.05 (p < .001 compared with patients with normal kidneys and p < .001 compared with patients with unilateral dilatation without obstruction). Patients with unilateral dilatation but without obstruction (n = 16) had a mean resistive index of 0.63 +/- 0.06 and a difference between kidneys of 0.06 +/- 0.04 (values within normal limits). The positive and negative predictive values of the obstruction criteria for unilateral collecting system dilatation were 95% and 100%, respectively. After successful surgical correction of ureteropelvic junction obstruction (n = 29), patients had a normal mean resistive index of 0.61 +/- 0.05 and a normal difference between kidneys of 0.03 +/- 0.03. Five patients examined both before and after surgery showed a statistically significant drop in the resistive index of the obstructed kidney (0.75 +/- 0.03 to 0.65 +/- 0.05, p < .05) after surgery and a small rise in the resistive index of the contralateral kidney (0.56 +/- 0.04 to 0.63 +/- 0.04, p < .02). CONCLUSION: The resistive index appears to be an effective parameter for the evaluation and follow-up of unilateral obstructive or nonobstructive ureteropelvic junction dilatation in children.

Adolescent↗
PubMed1992

Cardiac manifestations of cocaine abuse: a cross-sectional study of asymptomatic men with a history of long-term abuse of "crack" cocaine.

OBJECTIVES: The objective of this study was to evaluate the prevalence of cardiac abnormalities in young, asymptomatic long-term "crack" cocaine abusers. BACKGROUND: Although the cardiac complications of cocaine abuse have received widespread attention, the prevalence of cardiac abnormalities in asymptomatic long-term cocaine abusers is unknown. METHODS: History, physical examination, electrocardiogram (ECG) and echocardiogram were performed in 52 consecutive long-term cocaine abusers admitted to a drug rehabilitation program. Findings were compared with those in 14 age-matched normal volunteers and 14 age-matched normotensive patients admitted to a psychiatric service who had a pattern of smoking and alcohol consumption similar to that of the study patients. RESULTS: The ECG findings were abnormal in 29% of cocaine abusers, and included nonspecific ST-T wave changes in 15%, abnormal ST segment elevation in 10%, old inferior infarction in 2%, old anteroseptal infarction in 2% and abnormal precordial R wave progression in 10%. When compared with normal volunteers and control patients, cocaine abusers had increased left ventricular posterior wall thickness (1.12 vs. 0.76 and 0.85 cm, respectively, p < 0.0001), increased septal thickness (1.13 vs. 0.76 and 0.86 cm, p < 0.001) and higher left ventricular mass index (142 vs. 84 and 94 g/m2, p < 0.0001). Left ventricular diastolic filling variables did not differ significantly among the three groups. Diastolic filling variables were similar in cocaine abusers with and without left ventricular hypertrophy, and the prevalence of left ventricular hypertrophy did not differ significantly between those who used no alcohol or < 35 ml/week of alcohol and those who consumed > or = 500 ml/week of alcohol. Left ventricular segmental wall motion abnormalities were present in 11 subjects (21%) and the ejection fraction was decreased (< 0.45) in 2 (4%). CONCLUSIONS: Electrocardiographic and echocardiographic abnormalities are common in long-term cocaine abusers. Despite the frequent occurrence of left ventricular hypertrophy, Doppler-derived diastolic filling pattern was not altered. Concomitant alcohol use did not affect the prevalence of these abnormalities.

Age Factors↗
PubMed1992

Circadian rhythm of heart rate variability in survivors of cardiac arrest.

Reduced heart rate (HR) variability is associated with increased risk of cardiac arrest in patients with coronary artery disease. In this study, the power spectral components of HR variability and their circadian pattern in 22 survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction were compared with those of 22 control patients matched with respect to age, sex, previous myocardial infarction, ejection fraction and number of diseased coronary arteries. Survivors of cardiac arrest had significantly lower 24-hour average standard deviation of RR intervals than control patients (29 +/- 10 vs 51 +/- 15 ms, p less than 0.001), and the 24-hour mean high frequency spectral area was also lower in survivors of cardiac arrest than in control patients (13 +/- 7 ms2 x 10 vs 28 +/- 14 ms2 x 10, p less than 0.01). In a single cosinor analysis, a significant circadian rhythm of HR variability was observed in both groups with the acrophase of standard deviation of RR intervals and high-frequency spectral area occurring between 3 and 6 A.M. which was followed by an abrupt decrease in HR variability after arousal. The amplitude of the circadian rhythm of HR variability did not differ between the groups. Thus, HR variability is reduced in survivors of cardiac arrest but its circadian rhythm is maintained so that a very low HR variability is observed in the morning after awakening, corresponding to the time period at which the incidence of sudden cardiac death is highest.

Cardiac Catheterization↗
PubMed1992

Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm.

BACKGROUND: Silent myocardial ischemia in patients with coronary atherosclerosis is associated with an increased risk of adverse cardiac events, including sudden death. The relation between silent ischemia and the initiation of potentially fatal ventricular arrhythmias has not been defined, however. METHODS: As part of a long-term study of sudden cardiac death, data on arrhythmias, coronary anatomy, and responses to ergonovine testing to provoke coronary-artery spasm were collected prospectively among survivors of out-of-hospital cardiac arrest who had no flow-limiting coronary-artery lesions, prior myocardial infarctions, or other structural causes of cardiac arrest and no angina pectoris. Associations between silent myocardial ischemia due to coronary-artery spasm and the occurrence and characteristics of life-threatening ventricular arrhythmias were studied by both invasive and noninvasive techniques. RESULTS: Silent ischemic events were associated with the initiation of life-threatening ventricular arrhythmias in five patients with induced or spontaneous focal coronary-artery spasm (or both). These patients were identified among a group of 356 survivors of out-of-hospital cardiac arrest who were evaluated between 1980 and 1991. In two of the five patients reperfusion, rather than ischemia itself, correlated with the onset of the ventricular arrhythmia. Only one of the five had an inducible arrhythmia during electrophysiologic testing. Titration of the dose of a calcium-entry-blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested. CONCLUSIONS: Silent myocardial ischemia due to coronary-artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting structural coronary-artery lesions. The role of silent ischemia, reperfusion, or both in the initiation of fatal arrhythmias in larger groups of patients with advanced coronary-artery lesions remains to be defined.

Adult↗