Current role of digitalis therapy in patients with congestive heart failure.

Digitalis has been used in the treatment of chronic congestive heart failure for 215 years. In this article, numerous clinical studies and trials that have evaluated the efficacy of digitalis in the treatment of patients with congestive heart failure are reviewed. The data indicate that digitalis is a valuable therapeutic agent for relieving symptoms and improving exercise performance and left ventricular function in patients with congestive heart failure. Comparison of the various advantages and disadvantages of digitalis with alternative therapies in patients with congestive heart failure shows an important continuing role for digitalis therapy.

Coronary arteriography in the anginal syndromes.

Coronary arteriography maintains a major role in the management of patients with stable and unstable anginal syndromes, in the establishment of diagnosis and prognosis, and in guiding the choice of therapeutic alternatives. Included in this article are discussions of assessment of coronary artery disease, and coronary arteriography in patients with stable and unstable angina pectoris.

Risk stratification in survivors of acute myocardial infarction: routine cardiac catheterization and angiography is a reasonable approach in most patients.

Noninvasive risk assessment in survivors of AMI can effectively subdivide patients into groups with differing risk profiles after hospital discharge, but some patients at risk for late death or recurrent AMI may be incorrectly identified; data from cardiac catheterization and angiography provide complementary and generally more powerful prognostic information. Many patients may derive particular benefit from early cardiac catheterization and angiography, including: (1) patients with AMI complicated by recurrent myocardial ischemia, congestive heart failure, and/or complex ventricular arrhythmias; (2) patients with abnormal or inconclusive results of noninvasive testing or those patients unable to perform an exercise test; (3) patients with abnormal left ventricular global systolic function and those with increased left ventricular end-systolic volume; (4) "young" patients (younger than 50 years of age?); (5) older patients (older than 65 to 70 years of age?); (6) patients with non-Q wave AMI; and (7) patients who are receiving thrombolytic therapy. Performance of early cardiac catheterization and angiography in virtually all survivors of AMI, with selective use of appropriate noninvasive tests, may provide a more efficacious means of risk assessment after AMI; if all tests are performed judiciously, the cost of such an approach need not be excessive. A combination of invasive and selected noninvasive tests probably provides optimal information. The risks to the routine performance of diagnostic cardiac catheterization and angiography in all survivors of AMI are: (1) adequate care and attention may not be paid to proper performance of the procedure(s) and to detailed and proper analyses of the data; (2) the need for additional noninvasive testing in selected patients may be ignored; and most importantly, (3) premature or unnecessary revascularization procedures may be performed subsequently. For optimal patient care, the clinician must obtain all necessary data, avoid unnecessary and repetitive tests, know the accuracy of individual tests at his or her own facility, interpret all data in proper context, and then counsel patients objectively about available management strategies. With this approach, all patients who might appropriately benefit from coronary artery revascularization will be correctly identified, and patients who are truly at very low risk (minimal residual coronary artery disease and preserved left ventricular function particularly if associated with a patent infarct-related artery) may be similarly identified and managed appropriately with elimination of unnecessary additional testing and pharmacologic therapy. Finally, whatever approach to risk stratification one chooses for an individual patient, the importance of and the need to correct and/or ameliorate risk factors for coronary artery disease must be recognized and undertaken.

Effect of acute hemodynamic decompensation on electrical inducibility of ventricular arrhythmias in patients with dilated cardiomyopathy and complex nonsustained ventricular arrhythmias.

In patients with dilated cardiomyopathy, hemodynamic decompensation has been postulated to increase vulnerability to reentrant ventricular arrhythmias. To test this hypothesis, we performed programmed ventricular stimulation with three extrastimuli on nine patients with dilated cardiomyopathy and asymptomatic complex ventricular arrhythmias during a period of acute hemodynamic decompensation; programmed ventricular stimulation was then repeated following hemodynamic improvement with nitroprusside. These patients did not have a history of documented or suspected sustained ventricular tachycardia or fibrillation. The mean left ventricular ejection fraction was 0.21 +/- 0.04 (range 0.15 to 0.26). In the baseline state, mean right atrial pressure was 8 +/- 4 mm Hg, pulmonary artery wedge pressure was 20 +/- 3 mm Hg, and cardiac index was 3.2 +/- 0.5 L/min/m2. Following acute hemodynamic decompensation, mean right atrial pressure increased to 16 +/- 5 mm Hg and pulmonary artery wedge pressure to 33 +/- 8 mm Hg; cardiac index decreased to 2.1 +/- 0.5 L/min/m2. In this decompensated state, programmed ventricular stimulation failed to induce sustained or nonsustained ventricular arrhythmias in any patient. Following nitroprusside administration (mean dose 1.5 +/- 1.1 micrograms/kg/min), there were significant decreases in mean right atrial pressure (11 +/- 3 mm Hg) and pulmonary artery wedge pressure (16 +/- 3 mm Hg), and a significant increase in cardiac index (3.1 +/- 1.1 L/min/m2) (p less than 0.05 for all values versus the decompensated state). In the improved hemodynamic state, programmed ventricular stimulation induced nonsustained ventricular tachycardia (six beats) in only one patient, and sustained arrhythmias in none.(ABSTRACT TRUNCATED AT 250 WORDS)

Is noninvasive risk stratification sufficient, or should all patients undergo cardiac catheterization and angiography after a myocardial infarction?

From the foregoing discussion, it becomes apparent that although noninvasive risk stratification is a reasonable approach to assessment of patients following an uncomplicated myocardial infarction, the performance of early cardiac catheterization and angiography on nearly all such patients is not unreasonable and may in fact be the most practical approach. The basis for this rationalization may be summarized as follows: 1. Many subgroups will need early catheterization anyway a. Myocardial infarction complicated by recurrent ischemia, heart failure, or complex ventricular arrhythmias b. Patients receiving thrombolytic treatment c. "Young" patients (less than 50 years old?) d. "Older" patients (over ages 65 to 70?) in otherwise good medical condition e. Patients unable to exercise f. Patients with abnormal or inconclusive noninvasive test results (approximately 70 percent of patients) 2. Cardiac catheterization and angiography as a single test provides the two most powerful prognostic variables following myocardial infarction, namely, the extent of coronary artery disease and residual left ventricular function. This knowledge is reassuring to both physician and patient and allows for planning of optimal long-term management. 3. Certain limitations exist in noninvasive risk assessment strategies. 4. This approach need not be significantly more costly, if all tests are used wisely. The major risk inherent in the definition of the extent of coronary artery disease in all survivors of acute myocardial infarction might be the performance of unnecessary revascularization procedures (percutaneous transluminal coronary angioplasty or coronary bypass surgery). The burden rests with the individual clinician to (1) collect all useful and necessary data; (2) assess reliability and accuracy of various tests available at one's own institution; (3) avoid performing unnecessary and repetitive tests; (4) interpret the data in the proper context; and (5) counsel patients appropriately, correctly, and judiciously about their prognosis and therapeutic options. In this manner, all patients who might benefit appropriately from revascularization can be discovered early and offered this therapeutic option. Other patients can also be managed more appropriately; for example, those who are truly at very low risk (normal left ventricular function and either normal coronary arteries or "mild" coronary artery disease). However, it is most important to avoid unnecessary revascularization procedures. Although this discussion has focused on noninvasive and invasive testing following myocardial infarction, it is necessary to emphasize that comprehensive management of coronary artery disease and its complications should not be neglected in these patients; for example, control or amelioration of risk factors for coronary artery disease is mandatory in all these patients, and in their families as well.

Use of the internal mammary artery guiding catheter for percutaneous transluminal coronary angioplasty of the shepherd's crook right coronary artery.

Percutaneous transluminal coronary angioplasty (PTCA) of shepherd's crook right coronary arteries presents a difficult technical challenge. Presented here are two cases demonstrating the use of an internal mammary guiding catheter for PTCA of shepherd's crook right coronary arteries. The advantages of this guiding catheter, a short tip with an acute distal angle, are emphasized.

Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease.

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO4, serum magnesium rose significantly from 1.9 +/- 0.1 to 4.4 +/- 1.7 mg/dl (p less than 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 +/- 18 to 155 +/- 26 msec, p less than 0.05), AH interval (77 +/- 27 to 83 +/- 26 msec, p less than 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 +/- 67 to 293 +/- 67 msec, p less than 0.05), and sinoatrial conduction time (60 +/- 34 to 76 +/- 32 msec, p less than 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.

Central and renal hemodynamic effects and hormonal response to diltiazem in severe congestive heart failure.

The central and renal hemodynamic effects and the hormonal response to single doses of 60 mg and 90 mg of diltiazem were evaluated in 10 patients with severe chronic left ventricular (LV) systolic dysfunction (ejection fraction 0.22 +/- 0.08). Diltiazem administration resulted in only mild and mostly statistically insignificant changes. After 60 mg, only heart rate (from 86 +/- 10 beats/min at baseline to 79 +/- 14 beats/min at 4 hours) and pulmonary vascular resistance (from 231 +/- 108 to 165 +/- 74 dynes s cm-5 at 4 hours) changed significantly. Administration of 90 mg of diltiazem resulted in no significant change in any of the measured or calculated central hemodynamic variables. Individual data, however, revealed an increase stroke volume index in 3 patients but a decrease in 1 patient and a persistent increase in mean pulmonary artery wedge pressure in another patient. These hemodynamic changes were not associated with symptomatic deterioration in any of the patients. Both renal blood flow and glomerular filtration rate were impaired at baseline on both days and did not show a significant change 1, 2 and 4 hours after diltiazem administration. Similarly, no significant change was noted after either diltiazem dose in plasma catecholamine levels and renin concentration. In conclusion, administration of 60 to 90 mg of diltiazem in patients with severe chronic LV systolic dysfunction results in only mild and mostly insignificant acute effects on central and renal hemodynamics, plasma hormonal levels and patient clinical status.