ST-alternans alternans.
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Biomedical subjects
Publications and source records attributed to K M Kessler.
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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.
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.
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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.
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Sudden cardiac death (SCD) remains a major unresolved clinical and public health problem, accounting for more than 300,000 of the deaths in the United States annually. The ability to identify potential SCD victims is limited by the large size of the population subgroups that contain the majority of SCD victims and by the apparent time dependence of risk of sudden death. The latter refers to the tendency for SCD to follow other cardiovascular events within a high-risk period of 6-18 months after a primary cardiovascular event, with risk decreasing thereafter. The combination of time dependence and denominator pool size provides a basis for future studies to identify the higher risk individuals. Pathophysiologically, SCD can be viewed as an interaction between structural abnormalities of the heart, transient functional disturbances, and the specific electrophysiological events responsible for fatal arrhythmias. Structural abnormalities provide the anatomic substrate for chronic risk and include the myocardial consequences of coronary artery disease, left ventricular hypertrophy, myopathic ventricles, and specific electrophysiological anatomic abnormalities such as bypass tracts. The functional factors responsible for destabilizing a chronic electrophysiological abnormality include transient ischemia and reperfusion, systemic factors (e.g., electrolyte disturbances, acidosis, and hemodynamic dysfunction), autonomic fluctuations (both systemic and at a tissue level), and myocardial toxic influences such as proarrhythmic effects of various drugs. Each of these changes is able to destabilize myocardial membrane integrity, some regionally and some globally, making the heart susceptible to an electrical triggering event for ventricular tachycardia or fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular (LV) diastolic filling pattern of obese subjects with eccentric LV hypertrophy was studied. Findings were compared with those of normal control subjects and hypertensive patients with concentric LV hypertrophy. M-mode, 2-dimensional and Doppler echocardiograms were recorded in 11 obese (body mass index greater than 30 kg/m2) normotensive patients with eccentric LV hypertrophy, 10 normal control subjects, and 18 nonobese, hypertensive patients with concentric LV hypertrophy whose antihypertensive medications were discontinued 2 weeks before study. LV hypertrophy was defined as LV mass/height greater than 143 g/m. Hypertrophy in the obese patients was eccentric: Their LV internal dimension (61 +/- 3 mm) was greater than that of hypertensive patients (55 +/- 5 mm, p less than 0.001) and normal control subjects (55 +/- 2 mm, p less than 0.01); their septal (10.7 +/- 0.7 mm) and posterior (10.9 +/- 0.6 mm) wall thicknesses were smaller than those of the hypertensive patients (12.2 +/- 1.7 mm, p less than 0.05 and 11.7 +/- 1.2 mm, respectively, difference not significant). Pulsed-wave Doppler echocardiographic filling indexes were used to evaluate LV diastolic filling. Obese patients had a higher peak velocity of atrial filling (69 +/- 14 vs 54 +/- 15 cm/s, p less than 0.05), lower early/atrial filling velocity ratio (1.0 +/- 0.26 vs 1.32 +/- 0.21, p less than 0.05), prolonged deceleration half-time (108 +/- 9 vs 86 +/- 15 ms, p less than 0.01) and lower peak filling rate corrected to stroke volume (4.08 +/- 0.68 vs 4.96 +/- 0.88 stroke volume/s, p less than 0.05) than normal control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical outcome was analyzed among a group of 39 consecutive patients with coronary artery disease, left ventricular (LV) ejection fractions less than 30% and arrhythmias that required an automatic implantable cardioverter defibrillator (AICD) in an attempt to better define the role of the device in patients with severely depressed LV function. Twenty-nine (74%) were survivors of out-of-hospital cardiac arrest and 10 (26%) had ventricular tachycardia that was refractory to electrophysiologically guided antiarrhythmic therapy. The study group had the following demographic characteristics: 90% were men, mean age was 64 years (range 41 to 79) and mean LV ejection fraction was 21 +/- 4%. Concomitant pharmacotherapy included antiarrhythmic drugs 31 (79%), vasodilators in 22 (56%) and digoxin in 20 (51%). There was no statistical difference in baseline characteristics between survivors and nonsurvivors. Patients were followed for a mean of 24 months (range 2 to 72) from implantation. The difference between actuarial survival--77% at 1 year and 72% at 2 years--and projected survival without the AICD (patients who survive without appropriate device discharge)--30% at 1 year and 21% at 2 years--was significant (p less than 0.01 and less than 0.05 at 1 and 2 years, respectively). This study suggests that the AICD improves survival in patients with coronary artery disease despite severely depressed LV function.
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Coronary angioplasty of tortuous anomalous coronary arteries can be technically challenging. We describe a successful percutaneous transluminal coronary angioplasty (PTCA) of an anomalous right coronary artery after a failed previous attempt. The anatomic limitations of anomalous right coronary arteries and technical considerations for PTCA are discussed.
PURPOSE: Clinical and radiographic examinations are commonly used for estimating severity and titrating therapy of chronic congestive heart failure. The purpose of this study was to establish the relationship between findings on history, physical examination, chest roentgenogram, and pulmonary capillary wedge pressure (PCWP). PATIENTS AND METHODS: Fifty-two consecutive patients with chronic congestive heart failure, referred for evaluation for heart transplantation, were studied; all patients underwent history, physical examination, upright chest roentgenogram, and cardiac catheterization. The mean left ventricular ejection fraction was 0.19 +/- 0.06. Patients were divided into three groups according to their PCWP: Group 1, normal PCWP (less than or equal to 15 mm Hg, n = 19); Group 2, mild to moderately elevated PCWP (16 to 29 mm Hg, n = 15); Group 3, markedly elevated PCWP (greater than or equal to 30 mm Hg, n = 18). RESULTS: Physical and radiographic signs of congestion were more common in the groups with higher PCWP, but they could not be used to reliably separate patients with different filling pressures. Physical findings (orthopnea, edema, rales, third heart sound, elevated jugular venous pressure) or radiographic signs (cardiomegaly, vascular redistribution, and interstitial and alveolar edema) had poor predictive value for identifying patients with PCWP values greater than or equal to 30 mm Hg. These findings had poor negative predictive value to exclude significantly elevated PCWP (greater than 20 mm Hg). Radiographic pulmonary congestion was absent in eight (53%) patients in Group 2 and seven (39%) in Group 3. In patients in Group 2 and 3, those without radiographic congestion were in a better New York Heart Association functional class (3.5 +/- 0.5 versus 2.8 +/- 0.6, p less than 0.01). There was good correlation between right atrial pressure and PCWP (r = 0.64, p less than 0.001). A normal right atrial pressure had no predictive value, but a pressure greater than 10 mm Hg was seen in all but one patient with a PCWP value greater than 20 mm Hg. CONCLUSION: Clinical, radiographic, and hemodynamic evaluations of chronic congestive heart failure yield conflicting results. Absence of radiographic or physical signs of congestion does not ensure normal PCWP values and may lead to inaccurate diagnosis and inadequate therapy. It is not known whether therapy aimed at normalizing PCWP is superior to relieving clinical and radiographic signs of congestion.
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Right (RV) and left ventricular (LV) diastolic function was evaluated in 50 patients with mild, uncomplicated essential hypertension using pulsed-wave Doppler echocardiography. Patients with pulmonary, valvular or coronary artery disease were excluded and antihypertensive drugs were discontinued for the 2 weeks preceding the study. Ten normotensive patients without heart disease acted as control subjects. In the hypertensive patients, RV peak velocity of atrial filling was higher (42 +/- 10 vs 31 +/- 7 cm/s, p less than 0.01) and deceleration half-time was prolonged (96 +/- 20 vs 83 +/- 10 ms, difference not significant); ratio of early/atrial filling velocity (1.1 +/- 0.3 vs 1.7 +/- 0.4, p less than 0.001) and peak filling rate corrected to stroke volume (3.6 +/- 0.7 vs 5.3 +/- 0.9 SV/s, p less than 0.001) were lower. LV filling parameters showed similar changes. RV filling parameters did not correlate with age, LV mass or septal thickness but correlated weakly with LV radius/thickness ratio. There was good correlation between RV and the following corresponding LV filling parameters: peak filling rate, r = 0.68, p less than 0.001; ratio of early/atrial filling, r = 0.88, p less than 0.0001; and deceleration half-time, r = 0.62, p less than 0.001. Data indicate that RV diastolic function is abnormal in essential hypertension and these abnormalities are closely related to those of LV diastolic function.
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