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.

ST segment tracking for rapid determination of patency of the infarct-related artery in acute myocardial infarction.

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.

Serum levels of high-density lipoprotein phospholipids correlate inversely with severity of angiographically defined coronary artery disease.

In an attempt to assess the relationship between lipid abnormalities and severity of coronary artery disease, we measured serum levels of cholesterol (SC), triglycerides (TG), phospholipids (SP), low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), high density lipoprotein cholesterol (HDL-C), and high density lipoprotein phospholipids (HDL-P), in 217 men undergoing diagnostic coronary arteriography. We found significantly higher mean values of HDL-P and HDL-C in men with normal coronaries, but no significant differences in the other measured lipids. While there was no significant difference in HDL-C among patients with one, two or three-vessel disease, there was a negative correlation between HDL-P levels and the severity of the disease. These observations suggest that prospective studies would be of merit to establish the relevance of HDL-P in the development of coronary artery disease.

Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care.

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.

Are calcium antagonists proarrhythmic?

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.

Clinical usefulness and cost of echocardiography in patients admitted to a coronary care unit.

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.

Effects of hemodialysis on left ventricular diastolic filling.

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.

Right ventricular diastolic function in systemic hypertension.

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.

Abnormal left ventricular diastolic filling in eccentric left ventricular hypertrophy of obesity.

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)

Effect of clonidine on heart rate variability in congestive heart failure.

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.

Heart rate variability in inappropriate sinus tachycardia.

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.

Decreased heart rate variability in appropriate sinus tachycardia and effects of rapid rate.

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.

Usefulness of the automatic implantable cardioverter defibrillator in improving survival of patients with severely depressed left ventricular function associated with coronary artery disease.

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.

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)

Effect of hemodialysis on the signal-averaged electrocardiogram.

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.

Treatment of congestive heart failure. Its effect on pleural fluid chemistry.

The proper classification of pleural effusions into transudates and exudates has great clinical significance. It is believed that the treatment of congestive heart failure may convert an associated transudative pleural effusion into a "pseudoexudate." We studied eight patients with congestive heart failure during nine episodes of decompensation with pleural effusion, which was bilateral in five and right-sided in three. Thoracocentesis was done on identification of the patient and at 6 +/- 2 days after treatment of heart failure resulting in diuresis and a mean weight loss of 5.8 +/- 3.2 kg. The mean protein level of the pleural fluid was 2.2 +/- 0.7 g/dL at the initial study and increased to 3.2 +/- 1.08 g/dL at the final study (p less than 0.01). The LDH level of the pleural fluid increased from 116 +/- 69 to 183 +/- 117 units/L (p less than 0.01). The fluid/serum ratio for protein increased from 0.34 +/- 0.09 to 0.47 +/- 0.13 (p less than 0.01) and for LDH from 0.39 +/- 0.16 to 0.64 +/- 0.28 (p less than 0.01). In three patients, pleural fluid was classified as a transudate at the initial study but met the criteria for an exudate after treatment of heart failure. Effectiveness of diuresis was measured by weight loss; a significant correlation between weight loss per day and change in the protein level of the pleural fluid was noted (r = 0.715; p less than 0.05). We conclude that the treatment of congestive heart failure causes significant changes in the pleural fluid's chemistry; in some cases, a transudate may be converted into a "pseudoexudate."

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.

Iatrogenic internal mammary artery to coronary vein fistula.

Iatrogenic aortocoronary vein fistula following coronary artery bypass surgery is a rare complication. We describe the first reported case of inadvertent anastomosis of the left internal mammary artery to cardiac vein. The clinical characteristics and consequences as well as the angiographic characteristics of this fistula are described. Precautions that may be taken to prevent this complication are also addressed.

Reversible depression of myocardial performance in hypophosphatemia.

Studies of myocardial function in patients with hypophosphatemia have yielded conflicting results. Systolic time intervals were performed in 19 patients during and after the correction of hypophosphatemia; 11 had severe (0.9 +/- 0.15 mg/dL) and eight had moderate (1.4 +/- 0.11 mg/dL) hypophosphatemia. Controls were 14 patients with normal serum phosphorus levels. No patient with hypophosphatemia had clinical congestive heart failure. When hypophosphatemia was corrected, improvement in left ventricular performance was seen only in patients with severe hypophosphatemia (p less than 0.001); in eight patients left ventricular performance was normal during hypophosphatemia but showed significant improvement with its correction (p less than 0.01). Patients with moderate hypophosphatemia showed no significant change. Our results confirm the findings of O'Conner et al, whose study is the only previous one to demonstrate hypophosphatemia-induced myocardial depression in humans. Contradictory results from other studies may be explained by the inclusion of patients with moderate hypophosphatemia and failure to repeat measurements after the correction of hypophosphatemia. We conclude that reversible depression of myocardial performance is seen in hypophosphatemia only when it is severe. In some cases, normal left ventricular performance improves when hypophosphatemia is corrected.

Cardiac complications of cocaine abuse.

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.