L.David Hillis

Percutaneous transluminal coronary angioplasty

Percutaneous transluminal coronary angioplasty appears to be an effective alternative to coronary artery bypass surgery in patients whose coronary artery anatomy is suitable--that is, an individual with single (or, at most, double) vessel coronary artery disease whose stenoses are proximal, discrete, subtotal, concentric and noncalcified. Since emergent coronary artery bypass surgery is required in 5% to 7% of patients even when angioplasty is attempted by an experienced physician, the patient should be an acceptable candidate for surgery from both a cardiac and noncardiac standpoint. Unfortunately, ideal angioplasty candidates are a distinct minority among those with coronary artery disease. If the procedure is reserved for ideal (or nearly ideal) candidates, the rate of success should approach 75% to 80%, and the incidence of major complications should be below 10%. Although the procedure appears to be effective in alleviating angina, it is unlikely that it will exert a beneficial effect on survival when compared to either medical therapy or coronary artery bypass surgery.

Prognosis after acute myocardial infarction in patients with and without residual anterograde coronary blood flow

The restoration of anterograde coronary flow during the hours to days after acute myocardial infarction (AMI) may be beneficial independent of an effect on left ventricular function. This study was done to assess the influence of residual anterograde coronary perfusion on long-term morbidity and mortality in patients after AMI. Over a 10-year period, 179 subjects (132 men, 47 women, aged 25 to 66 years) with infarction and angiographic evidence of disease of only 1 coronary artery were followed for 47 +/- 29 (mean +/- standard deviation) months. All were receiving medical therapy. Sixty-four patients had partial or complete anterograde perfusion of the infarct artery (group I), whereas the other 115 had no or minimal anterograde perfusion (group II). The 2 groups were similar in age, sex, risk factors for atherosclerotic cardiovascular disease, duration of follow-up, maintenance medications and left ventricular function. In group I, unstable angina and congestive heart failure each occurred in less than or equal to 10%, and none died. In marked contrast, the 115 patients in group II frequently had unstable angina (25%) and congestive heart failure (17%) (p less than or equal to 0.05 for both vs group I), and 21 (18%) died suddenly (p less than 0.001 vs group I). Thus, the incidence of long-term morbidity and mortality is greatly increased after AMI in patients without residual anterograde perfusion of the infarct-related coronary artery. In these patients, the restoration of partial or complete anterograde flow--pharmacologically or mechanically--may be beneficial even if it is accomplished hours to days after the acute event.

Influence of labetalol on cocaine-induced coronary vasoconstriction in humans

PURPOSEnAlthough labetalol is sometimes given to patients with cocaine-associated chest pain, its influence on cocaine-induced coronary vasoconstriction is unknown.nnnPATIENTS AND METHODSnIn 15 patients (7 men, 8 women, aged 40 to 79 years) undergoing catheterization for chest pain, heart rate, mean arterial pressure, and coronary arterial area (by computer-assisted quantitative angiography) were measured (1) at baseline, (2) 15 minutes after intranasal cocaine, 2 mg/kg, then (3) 5 minutes after intravenous saline (n = 6) or labetalol, 0.25 mg/kg (n = 9).nnnRESULTSnOf 40 coronary arterial segments analyzed, cocaine induced a 13% +/- 10% (mean +/- standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 +/- 14 mm Hg after cocaine, 110 +/- 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 +/- 1.37 mm2 after cocaine, 3.37 +/- 1.32 mm2 after labetalol; p = NS).nnnCONCLUSIONnLabetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.

Continuous electrocardiographic monitoring in patients with unstable angina pectoris: Identification of high-risk subgroup with severe coronary disease, variant angina, and/or impaired early prognosis

We assessed the value of two-channel Holter monitoring during the initial hours of hospitalization in patients with unstable angina pectoris (UAP) to identify those with severe coronary artery disease (CAD), variant angina, and/or poor prognosis over the next 3 months. Accordingly, 116 UAP patients had Holter monitoring for 27 +/- 7 (mean +/- SD) (range 12 to 50) hours following hospitalization. Of these, 24 evolved myocardial infarction (MI) during monitoring and 92 did not. Transient ST segment alterations occurred in 21 of the 92. Of these 21, 4 had variant angina, were treated with calcium antagonists, and did well. Each of the remaining 17 had severe fixed CAD (left main or three-vessel) (n = 12) and/or poor prognosis over the 3 months after discharge as manifested by death (n = 1), MI (n = 3), and/or severe angina (n = 3). In contrast, 71 patients did not demonstrate transient ST segment alterations: none had variant angina (p less than 0.001), nine had left main or three-vessel CAD (p less than 0.001), and 50 were alive and well 3 months after discharge (p less than 0.001). Ventricular tachycardia (VT) was demonstrated by Holter monitor in 5 of the 92 patients: four had three-vessel CAD and the other had severe persistent angina. Thus in patients hospitalized with unstable angina, transient ST segment alterations and/or VT on Holter monitor are specific predictors of high-risk subgroup UAP patients with left main or three-vessel CAD, variant angina, and/or impaired 3-month prognosis.

Alleviation of cocaine-induced coronary vasoconstriction by nitroglycerin

Cocaine induces vasoconstriction of epicardial coronary arteries in patients with and without coronary artery disease, and this vasoconstriction is particularly marked in segments narrowed by atherosclerosis. To assess the effect of nitroglycerin on cocaine-induced coronary vasoconstriction, computer-assisted quantitative analysis was performed on non-diseased and diseased coronary artery segments in 23 patients (18 men, 5 women, aged 43 to 65 years) 1) at baseline, 2) after administration of intranasal saline solution (in 8 patients) or 2 mg/kg of cocaine (in 15 patients), and then 3) after administration of sublingual placebo (in 6 patients) or 0.4 or 0.8 mg of nitroglycerin (in 9 patients) in the 15 patients given cocaine. In response to cocaine administration, coronary artery cross-sectional area decreased 22 +/- 7% (mean +/- SD) in non-diseased segments (p less than 0.05) and 45 +/- 18% in diseased segments (p less than 0.02). The magnitude of vasoconstriction was greater (p = 0.01) in the diseased segments. Sublingual nitroglycerin abolished the vasoconstriction in both non-diseased and diseased segments. Thus, nitroglycerin alleviates cocaine-induced vasoconstriction in patients with coronary artery disease.

The natural history of isolated left ventricular diastolic dysfunction.

STUDY OBJECTIVEnTo assess the natural history of isolated left ventricular diastolic dysfunction.nnnPATIENTS AND METHODSnFollow-up (average duration, 68 months) was obtained in 51 patients with isolated left ventricular diastolic dysfunction at cardiac catheterization, characterized by (1) an elevated left ventricular end-diastolic pressure; (2) normal left ventricular end-diastolic and end-systolic volumes; (3) normal left ventricular ejection fraction; (4) no coronary artery disease; and (5) no valvular disease.nnnRESULTSnDuring follow-up, seven patients died, but only one died of cardiac causes. Of the 44 living subjects, 20 (45%) noted new-onset symptoms of congestive heart failure, with 11 (25%) of these requiring hospitalization, and 12 (27%) required hospitalization for recurrent chest pain.nnnCONCLUSIONSnIsolated left ventricular diastolic dysfunction is associated with a low cardiac mortality; at the same time, however, it is associated with substantial morbidity.

Influence of anterograde flow in the infarct artery on the incidence of late potentials after acute myocardial infarction

In patients after myocardial infarction, survival is influenced by the presence or absence of anterograde flow in the infarct artery, and late potentials on signal-averaged electrocardiography identify those at risk for tachyarrhythmias and sudden death. To assess the frequency of late potentials in survivors of first infarction, coronary arteriography and signal-averaged electrocardiography were performed in 109 subjects (64 men, 45 women, aged 30 to 77 years), 49 with (group I) and 60 without (group II) anterograde flow in the infarct artery. The groups were similar in age, sex, infarct artery, severity of coronary artery disease and left ventricular function. However, only 4 (8%) of group I had late potentials, whereas 24 (40%) of group II had late potentials (p less than 0.001). Thus, anterograde flow in the infarct artery after myocardial infarction is associated with a low incidence of late potentials on signal-averaged electrocardiography, whereas the absence of anterograde flow is more often associated with late potentials.

Hemodynamic and electrophysiologic effects of verapamil and nifedipine in patients on propranolol

Abstract Because the combined use of a beta-adrenergic blocking agent and a calcium antagonist may be beneficial in patients with severe angina, we assessed the hemodynamic and electrophysiologic effects of verapamil or nifedipine in patients receiving oral propranolol. In 26 patients with stable angina receiving oral propranolol (234 ± 230 mg/day, mean ± standard deviation), cardiac catheterization was performed, and variables were measured at baseline and 5 to 10 minutes after (1) intravenous saline solution, 10 ml (n = 6); (2) intravenous verapamil, 0.15 mg/kg body weight to a maximal dose of 10 mg (n = 10); and (3) sublingual nifedipine, 10 mg (n = 10). Cardiac output (by thermodilution) was unchanged after saline solution and verapamil but increased with nifedipine (4.3 ± 1.1 to 5.0 ± 1.4 liters/min, p

Direct measurement of cardiac output by gated equilibrium blood pool scintigraphy: Validation of scintigraphic volume measurements by a nongeometric technique

Abstract A nongeometric technique for the determination of left ventricular volumes from the count data derived from gated equilibrium blood pool scans was previously described and validated by the demonstration of an excellent correlation between the derived data and angiographically determined left ventricular volumes. To provide a further prospective evaluation of this method and to validate its ability to determine stroke volume and cardiac output by a technique that is itself independent of geometric assumptions, simultaneous measurements of cardiac output by the thermodilution technique and gated scintigraphy were performed in 21 patients without valve regurgitation or intracardiac shunts. To substantiate the reliability of scintigraphic measurements at high levels of cardiac output, seven patients had multiple measurements of cardiac output at rest and during an infusion of isoproterenol. There was an excellent correlation between thermodilution and scintigraphic values for cardiac output (scan cardiac output = 0.99 thermodilution cardiac output − 0.005 liters/min; n = 31, standard error of the estimate [SEE]= 0.175 liters/min, r = 0.97) as well as between thermodilution and scintigraphic stroke volumes (scan stroke volume = 1.03 thermodilution stroke volume − 2.8 ml; n = 31, SEE = 2.5 ml, r = 0.95). In addition, the relation between scintigraphic and angiographic measurements of left ventricular volumes continued to be excellent: In 15 patients with technically adequate angiograms, scintigraphic left ventricular volume = 0.90 angiographic left ventricular volume + 7 ml (n = 30, SEE = 10 ml, r = 0.91). Thus, this study further validates the nongeometric method of measuring left ventricular volumes with gated scintigraphy and demonstrates its ability to measure left ventricular stroke volume and cardiac output reliably.

Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia

Atrial pacing has been used to assess the physiologic impact of coronary artery disease (CAD). Several variables have served as markers of pacing-induced myocardial ischemia, but their specificities and sensitivities are unknown. Accordingly, in 28 patients, incremental atrial pacing was performed. Of the 28, 10 had no CAD. The left ventricular ejection fraction (LVEF) (by gated equilibrium blood pool scintigraphy) increased in this group (0.60 +/- 0.11 [mean +/- standard deviation] before pacing to 0.67 +/- 0.13 at peak-pacing, p = 0.002). In no patient did left ventricular end-diastolic pressure increase by greater than 5 mm Hg. No patient had lactate production, and 2 (20%) had electrocardiographic S-T segment depression greater than or equal to 0.1 mV. Four (40%) had chest pain with atrial pacing. In the remaining 18 patients with CAD, atrial pacing caused a decrease in LVEF greater than or equal to 0.05 (0.46 +/- 0.10 to 0.33 +/- 0.09, p less than 0.001) and new segmental wall motion abnormalities in all, indicating pacing-induced myocardial ischemia. Only 8 (44%) had an increase in left ventricular end-diastolic pressure of greater than 5 mm Hg, and only 9 (50%) had lactate production. Ten (56%) had ischemic electrocardiographic changes, and 12 (67%) had chest pain. Thus, the electrocardiographic, metabolic, and hemodynamic alterations that may accompany pacing-induced ischemia are specific but relatively insensitive markers of ischemia. In contrast, chest pain during atrial pacing is a nonspecific occurrence, appearing with similar frequency in normal subjects and patients with CAD and pacing-induced ischemia.