Group C streptococcal endocarditis associated with intubation-induced tracheal stenosis

We describe a 44-year-old woman with Group C haemolytic streptococcal endocarditis who developed tracheal stenosis as a result of endotracheal intubation. She recovered fully following valve replacement for continuing left ventricular failure due to mitral and aortic incompetence and subsequent resection of the stenosed tracheal segment with reanastomosis of the trachea.     

Aortic valve endocarditis complicated by complete heart block

A 34-year-old man with severe aortic incompetence caused by Streptococcus viridans developed severe central chest pain followed by complete heart block, multifocal ventricular extrasystoles, lengthening of the QTc and signs of cerebral emboli and pulmonary oedema. Early antibiotic therapy along with pacing, non-invasive investigations coupled with early surgery contributed significantly to the patient's survival.     

Q-T prolongation and polymorphous (“torsade de pointes”) ventricular arrhythmias associated with organophosphorus insecticide poisoning

It is not generally appreciated in the Western world that organophosphorus poisoning may be associated with a serious and often fatal cardiac complication: Q-T interval prolongation with malignant ventricular arrhythmias of the “torsade de pointes” type. This Insidious complication may lead to delayed, sudden death after the patient appears to be well on the way to recovery from the other, more dramatic respiratory and neurologic symptoms. In this study 15 patients with organophosphorus poisoning are described. Q-T prolongation was observed in 14 and malignant tachyarrhythmlas in 6. In view of the dismal prognosis of these patients, ventricular pacing, previously used with success In other conditions associated with this syndrome, was tried in four patients and successfully shortened the Q-T interval and eliminated the arrhythmias. Isoproterenol did the same in a fifth patient. Awareness of this lethal, but preventable complication of organophosphorus poisoning is called for. Careful electrocardiographic monitoring is necessary until the Q-T interval returns to normal. Electrical pacing appears to be the treatment of choice for the tachyarrhythmias.     

Polymorphous ventricular tachycardia associated with normal and long Q-T intervals

Polymorphous ventricular tachycardia may occur in the setting of either a normal or a prolonged Q-T interval. Torsade de pointes is a form of polymorphous ventricular tachycardia in which the polarity of the QRS complex exhibits phasic alterations in both axis and rate. Traditionally, torsade de pointes has been described in association with a variety of congenital and acquired (including drug and metabolic) causes of Q-T prolongation. The distinction between torsade de pointes and those polymorphous ventricular tachycardias occurring in patients with a normal Q-T interval has important therapeutic implications. The former requires strict avoidance of all drugs that may potentially further delay repolarization, including class I antiarrhythmic agents; immediately, the initiation of cardiac pacing is often necessary for control of arrhythmia, and on a long-term basis, sympathetic nervous blockade is often efficacious. In contrast, the polymorphous ventricular tachycardias with a normal Q-T interval usually respond to conventional therapy, including administration of class I antiarrhythmic agents. Thus, the management of polymorphous ventricular tachycardia should be based on the presence or absence of associated repolarization alterations rather than on the morphologic features of the tachycardia. Unfortunately, recent advances in basic and clinical electrophysiology have not yet elucidated the pathophysiologic basis for these arrhythmias, although this is an area of active investigative interest.     

Hemodynamic effects of encainide in patients with ventricular arrhythmia and poor ventricular function

Gated cardiac scanning was used to evaluate the hemodynamic effects of encainide in 19 patients (1 woman) with complex ventricular arrhythmia and depressed left ventricular (LV) function (ejection fraction less than 45%). Patients were 36 to 80 years old (average 61). All were candidates for long-term encainide therapy after having failed with currently available antiarrhythmics. Sixty-three percent had congestive heart failure before they received encainide. All were evaluated in the hospital before encainide therapy by a gated cardiac scan performed at least 3 days after discontinuing all antiarrhythmic drugs. Patients received oral encainide in doses of 75 to 200 mg. Gated cardiac scans were repeated 1 to 2 weeks later when an 80% reduction in frequency of premature ventricular complexes was observed on a 24-hour Holter recording. No patient had worsening of congestive heart failure during encainide therapy. Encainide did not significantly affect ejection fraction, which averaged 22 +/- 10% before and 25 +/- 14% (SD) after encainide (difference not significant [NS]). Other hemodynamic variables, including heart rate, blood pressure, stroke volume and end-diastolic volume, remained unchanged during encainide therapy. Digoxin blood levels in 10 patients averaged 1.04 +/- 0.43 before and 1.22 +/- 0.47 mg/ml (NS) during encainide therapy. Thus, encainide given orally in clinically effective doses does not appear to have significant hemodynamic effects in patients with ventricular arrhythmia and depressed LV function.     

The effects of practolol on the dysrhythmias complicating acute ischemic heart disease

The cardioselective beta-adrenoceptor blocking agent practolol was used in the management of ventricular and supraventricular dysrhythmias associated with acute myocardial Infarction in 134 patients, and in the management of these dysrhythmias in 19 patients with acute myocardial ischemia. Practolol was frequently effective in controlling ventricular dysrhythmias which occurred within the first 24 hours after the onset of symptoms of acute myocardial infarction. It was also effective in controlling the ventricular dysrhythmias which occurred after resuscitation from ventricular fibrillation. It was of particular value when therapeutic doses of lidocaine had been ineffective. Practolol was much less effective in controlling ventricular dysrhythmias which occurred more than 24 hours after acute infarction. Atrial fibrillation and atrial flutter were infrequently abolished by practolol in undigitalized patients after acute myocardial infarction. There was no correlation between the effectiveness of practolol and the blood concentration of the drug. One adverse effect of practolol was the occurrence of sinus bradycardia with or without an increase in the frequency of ventricular ectopic beats. Bradycardia was sometimes accompanied by hypotension. Severe hypotension occasionally occurred in the absence of bradycardia.     

Nature of inducible ventricular tachyarrhythmias in a canine chronic myocardial infarction model

A canine model suitable for serial conscious studies was developed to evaluate the nature of sustained ventricular tachyarrhythmias in chronic experimental myocardial infarction. Thirteen dogs underwent left anterior descending coronary artery ligation followed by complete reperfusion; 11 sham-operated dogs served as controls. In this model, ventricular tachyarrhythmias are inducible in most dogs with experimental infarction and in several dogs without this condition. The morphologic features, rate and drug response of the induced arrhythmias are unlike those of human ventricular tachycardia. Tachyarrhythmia induction is facilitated by anesthesia and thoracotomy. This canine infarct model does not adequately imitate human recurrent ventricular tachycardia, but may simulate human sudden cardiac death.     

Effects of negative pleural pressure on left ventricular hemodynamics

Negative pleural pressure alters left ventricular (LV) function. LV volume changes have been studied in human subjects, but little is known of the hemodynamic effects. The effect of changes of pleural pressure on LV hemodynamics during a Mueller maneuver (inspiration against an obstruction) was studied in 11 subjects and during quiet, unobstructed inspiration in 3. During the Mueller maneuver, there was an initial decrease in pulmonary wedge pressure and aortic systolic pressure, almost as great as the decrease in pleural pressure. Thereafter, these pressures increased despite a sustained reduction in pleural pressure. Toward the end of the Mueller maneuver, pulmonary wedge transmural pressure averaged 31 ± 12 mm Hg and in 6 patients large v waves developed. The increase in aortic transmural pressure averaged 30 ± 16 mm Hg. Aortic pulse pressure decreased on the first beat from control levels of 59 ± 21 to 47 ± 21 (p < 0.001) and then returned to control levels.During normal breathing in 3 subjects, studied with intraesophageal balloons, there was a similar increase in both transmural aortic and transmural pulmonary wedge pressures with a decrease in pleural pressure 6 mm Hg during inspiration.Thus, increased negative pleural pressure was associated with a marked increase in pulmonary wedge transmural pressure; the increase was approximately proportionate to the decrease in pleural pressure. It is suggested that this increase was due to increased impedance to LV ejection and to right ventricular expansion interfering with LV diastolic filling.     

Efficacy of verapamil in chronic, recurrent ventricular tachycardia

Verapamil, 0.25 mg/kg, was given to 24 patients with chronic, recurrent ventricular tachycardia (VT) whose clinical tachyarrhythmias were reproduced at electrophysiologic study. Seven patients (29%) responded acutely to verapamil: VT was not inducible in 5 and spontaneously terminated within 5 seconds of induction in 2 patients in whom it was previously sustained. Four of the 7 responders had no identifiable structural heart disease, and 3 had coronary artery disease. Responders were younger and had better left ventricular function than did nonresponders. Long-term therapy with verapamil, attempted in 5 of the 7 responders, was effective in 3, ineffective in 1, and of uncertain efficacy in 1. Verapamil therapy was discontinued because of worsened congestive heart failure in 2 patients.

The short-term efficacy of verapamil in these patients compares favorably with the efficacy of other antiarrhythmic agents against VT induction in patients with long-term, recurrent, drug-refractory VT. The short-term efficacy of verapamil correlated with its long-term efficacy. These observations provide preliminary evidence that verapamil may be useful in the treatment of some patients with recurrent VT. When standard drugs are not effective, verapamil should be given a trial, especially in young patients with good left ventricular function.     

Determinants of the outcome of electrophysiologic study in patients with ventricular tachyarrhythmias

To determine those factors predictive of the ability to both initiate and suppress ventricular tachyarrhythmias during electrophysiologic study, the results of programmed cardiac stimulation were evaluated in 261 patients: 66 presenting with nonsustained ventricular tachycardia, 91 with sustained ventricular tachycardia and 104 with ventricular fibrillation. Multivariate logistic regression analysis revealed that the presenting arrhythmia was a potent and independent predictor of the ability to provoke ventricular arrhythmias at electrophysiologic study; a history of myocardial infarction and male sex were also significant independent predictors. Of patients presenting with sustained ventricular tachycardia, 89% (81 of 91) had inducible ventricular arrhythmias compared with 61 (40 of 66) and 66% (69 of 104) of patients with nonsustained ventricular tachycardia and ventricular fibrillation, respectively. Complete suppression of inducible arrhythmias could be achieved in only 52% (34 of 66) of patients with sustained ventricular tachycardia, compared with 73 (24 of 33) and 75% (46 of 61) of patients presenting with nonsustained ventricular tachycardia and ventricular fibrillation, respectively. Multivariate analysis showed that the major independent determinants of the ability to suppress inducible arrhythmias were the number of drug trials performed before electrophysiologic study (inversely correlated) and the nature of the induced arrhythmia. The nature of the presenting clinical arrhythmia is, therefore, a highly significant and independent predictor of the ability to induce ventricular arrhythmias during electrophysiologic testing and an important determinant of the ability to suppress induced arrhythmias in patients with spontaneous ventricular tachyarrhythmias.     

Eosinopenia as an Adverse Marker of Clinical Outcomes in Patients Presenting with Acute Myocardial Infarction

BackgroundEosinopenia is considered a surrogate of inflammation in several disease settings. Following ST-segment elevation myocardial infarction, eosinopenia is presumed to be a marker of infarct severity. We sought to study the relationship between eosinopenia and infarct severity and how this relationship determined the long-term outcomes following ST-segment elevation myocardial infarction.MethodsSix hundred and six consecutive patients undergoing primary percutaneous coronary interventions from a large volume single center were enrolled. Low eosinophil count was defined as < 40 cells/mL from samples within 2 hours after reperfusion. Primary endpoint was defined as composite of death, myocardial infarction, stroke, unplanned revascularization, and readmission for heart failure over 3.5 years’ follow-up.ResultsSixty-five percent of the patients had eosinopenia. Patients in the low eosinophil group had larger infarct size as measured by troponin value (2934 vs 1177 ng/L, P < .001) and left ventricle systolic function on echocardiography (48% vs 50%, P = 0.029). There was a weak correlation between eosinophil count and both troponin (r = -0.25, P < 0.001) and ejection fraction (r = 0.10, P = .017). The primary endpoint was higher in eosinopenic patients (28.8% vs. 20.4%; hazard ratio [HR] 1.49, 95% confidence interval [CI] 1.05 to 2.13, P = .023). A discordance between eosinopenia and severe left ventricle systolic dysfunction was observed in 55.6% of cases. Compared with normal count, eosinopenia was associated with worse clinical outcomes in patients with non-severe left ventricle dysfunction (24.1% vs 16.2%; HR 1.58, 95% CI 1.01 to 2.45, P = .044) but not in those with severe left ventricle dysfunction (42.3% vs. 38.9%; HR 1.10, 95% CI 0.59 to 2.03, P = .77) (P < .01 for interaction).ConclusionsEosinopenia is an easily determined marker that reflects worse clinical outcomes over long-term follow-up.     

Surgery for life-threatening ventricular tachyarrhythmias.

Among 203 left ventricular aneurysmectomies performed since 1970, the operative mortality rate was 18.7 percent. In 49 patients (24 percent), left ventricular aneurysmectomy was performed for refractory life-threatening ventricular arrhythmias. Eight additional patients had coronary bypass grafting without ventricular aneurysmectomy. One of these patients had bypass grafting followed later by ventricular aneurysmectomy. All 56 patients had underlying coronary artery disease. The operative mortality rate was 19.6 percent. In patients with a recent myocardial infarction, the rate was 60 percent, whereas it was 11 percent in patients with a remote myocardial infarction. Other high risk variables in these patients included coronary bypass grafting without myocardial resection, and an elevated left ventricular end-diastolic pressure. The late mortality rate was 17.9 percent, but only one of these deaths was sudden and unexpected. The 35 long-term survivors have been followed up for a mean of 40.7 months (range 7 to 92 months). Of these, 20 remain on antiarrhythmic medications for palpitation or documented ventricular premature complexes, whereas 15 are free of detectable rhythm disturbances and do not require antiarrhythmic agents. Only 4 of 35 (11 percent) have had recurrent documented ventricular tachycardia. Left ventricular aneurysmectomy may be performed for refractory ventricular tachyarrhythmias with an acceptable operative mortality, particularly if the patient has survived longer than 6 weeks after myocardial infarction. Although epicardial mapping techniques may be useful in localizing the reentrant pathway of the ventricular tachycardia, ventricular aneurysmectomy without mapping techniques produces a satisfactory clinical result in the vast majority of long-term survivors.     

Management of intractable ventricular tachyarrhythmias after myocardial infarction.

Twenty-five patients with recent or old myocardial infarction were studied because they had life-threatening ventricular arrhythmias that required repeated cardioversions and were intractable to medical management. All patients had had a large anterior infarction a mean of 4.6 weeks before the emergence of the arrhythmias and all had severe left ventricular dysfunction. Cardiac catheterization or autopsy revealed a left ventricular aneurysm in 18 of 18 patients and obstruction of the left anterior descending coronary artery in 20 of 20 patients. Of 16 patients treated surgically with aneurysm resection or coronary bypass grafting, or both, 10 (62 percent) were alive after 3 to 39 (mean 26) months of follow-up. The perioperative mortality rate was 31 percent and only one patient died during the postoperative follow-up period 4 months after discharge from the hospital. By contrast, all nine medically treated patients died either in the hospital (four patients) or suddenly within 2 months of discharge (five patients). Ventricular fibrillation was documented as the cause of death in five of these patients. Surgical intervention was found to improve significantly the survival of these patients (P less than 0.02). The perioperative mortality rate was lower when at least 4 weeks had elapsed from acute infarction to surgery (10 versus 67 percent) and when the procedure included coronary bypass grafting (13 versus 50 percent), although these differences were not statistically significant (P greater than 0.05).     

Control of tachyarrhythmias associated with Wolff-Parkinson-White syndrome by amiodarone hydrochloride

Amiodarone hydrochloride proved to be highly effective in preventing and treating arrhythmias of the Wolff-Parkinson-White (WPW) syndrome in 11 patients with WPW conduction and recurrent tachyarrhythmias. Paroxysmal supraventricular tachycardia (six patients), atrial fibrillation (four patients) and atrial flutter (one patient) were the most significant arrhythmias. In most patients the arrhythmia was seriously disabling because of the extremely rapid ventricular rate, adverse hemodynamic consequences and frequent recurrence and long duration of the episodes. Other known antiarrhythmic agents were ineffective. In all 11 patients amiodarone, in doses of 300 to 600 mg daily, totally, easily and safety controlled the arrhythmias for periods of 2 to 8 months. The drug was fully effective after an average of 7 days of treatment. Tolerance to amiodarone was excellent. The occurrence of corneal microdeposits of the drug was the only Important undesirable effect, but subjective ocular disturbances were not noted. The microdeposits are reversible, and can be avoided by discontinuing the drug for 7 days every 1 to 2 months. Amiodarone apparently causes a significant prolongation of refractoriness in the normal (A-V node and His-Purkinje system) as well as in the anomalous pathway, thus creating favorable conditions for prevention and Interruption of any reentry mechanism requiring participation of both pathways.     

Normal left ventricular systolic function in adults with atrial septal defect and left heart failure

Systolic left ventricular contractile function has not been extensively evaluated in patients with atrial septal defect who have symptoms of left-sided congestive heart failure. This study examined left ventricular systolic function hemodynamically and angiographically in 6 such adult patients (Group A), 12 adult patients with atrial septal defect without heart failure (Group B) and 20 normal subjects. The mean (± standard error of the mean) left ventricular end-diastolic pressure was higher in patients in Group A (17 ± 0.8 mm Hg) than in patients in group B (6.9 ± 0.6 mm Hg) (p < 0.001). Both right atrial pressure (11 ± 1.3 versus 4.9 ± 0.5 mm Hg) (p < 0.001) and mean pulmonary arterial pressure (30 ± 1.8 versus 15 ± 1 mm Hg) were also higher in Group A than in Group B. Left ventricular cardiac index and stroke work index did not differ in the two groups.

Variables of left ventricular systolic function were similar in both groups of patients and in normal subjects: Ejection fraction was 0.71 ± 0.05 in Group A, 0.74 ± 0.02 in Group B and 0.74 ± 0.01 in normal subjects. Velocity of circumferential shortening was 1.38 ± 0.14 circumferences/s in Group A, 1.38 ± 0.07 circumferences/s in Group B and 1.27 ± 0.04 circumferences/s in normal subjects. There was no difference in left ventricular contractile function as indicated by the ratio of end-systolic wall stress to end-systolic volume index among the three groups: normal subjects, average 5.6 ± 0.19 versus 6.1 ± 0.5 in Group B and 6.0 ± 0.6 dynes × 10³/cm²/(ml/m²) in Group A.

This study of patients with atrial septal defect and left heart failure indicates that abnormal left ventricular systolic contractile function is probably not the cause of the symptoms and elevated left heart filling pressures observed in this group. An abnormality in left ventricular diastolic filling, perhaps related to the volume loaded right ventricle, may explain these changes.