James A. Joye

Combined dopamine and nitroprusside therapy in congestive heart failure. Greater augmentation of cardiac performance by addition of inotropic stimulation to afterload reduction.

The hemodynamic benefits of combining administration of dopamine with nitroprusside (NP) were evaluated in nine patients with chronic congestive heart failure due to ischemic, idiopathic myocardial or valvular cardiac disease. NP alone (68 μg/min) produced decline in left ventricular end-diastolic pressure (LVEDP) from 25.4 to 14.1 mm Hg (P < 0.01) but modest increase in cardiac index (CI) from 2.41 to 3.02 L/min/m2 (P < 0.05). Dopamine alone (6 μg/kg/min) caused an elevation of CI to 3.36 (P < 0.01) but without decrease of LVEDP. Simultaneous infusion of the two agents resulted in favorable alterations in both hemodynamic variables: LVEDP decreased to 15.7 (P < 0.01) and CI increased to 3.52 (P < 0.01). It is concluded that dopamine substantially enhances the effectiveness of nitroprusside therapy in congestive heart failure by providing concomitantly the principal beneficial actions of the vasodilator and dopamine used separately. Thus combined dopamine with NP treatment considerably raises low CI while markedly reducing elevated LVEDP and provides a potentially efficacious pharmacologic modality for the treatment of severe congestive heart failure due to left ventricular dysfunction.

Value and limitations of cross-sectional echocardiography of the aortic valve in the diagnosis and quantification of valvular aortic stenosis.

Few data are available regarding cross-sectional echocardiography (2-D) in the diagnosis and quantification of valvular aortic stenosis. Therefore, we compared echographic measurements obtained by 2-D echo with aortic gradient and aortic valve area and index calculated by the Gorlin formula in 20 normal subjects and 85 patients with clinical evidence of aortic stenosis. Technically adequate echograms were obtained in 72 patients (85%). Forty-six patients with satisfactory echograms were classified as having critical aortic stenosis, while 26 were designated as having noncritical obstruction. Aortic leaflet separation (SEP) was measured as the maximal intercusp distance visualized in either long, apical or short axis of the 2-D echo. SEP was less in critical aortic stenosis patients than in normal subjects and those with noncritical aortic stenosis (4.6 ± 0.4, 19.4 ± 0.5, and 10.0 ± 0.8 mm, respectively [mean ± SEMI [both p < 0.0011) and was greater than 15 mm in all normal subjects and 11 mm or less in all patients in the critical group. SEP correlated poorly with peak systolic gradient and calculated aortic valve area and index in aortic stenosis patients. Forty-two of 46 patients in the critical group had SEP of 8 mm or less, yielding a sensitivity of 91%. However, only 17 of 26 patients with noncritical aortic stenosis had a SEP of greater than 8 mm, for a specificity of 65%. Therefore, the predictive value of SEP 8 mm or less on 2-D echo in the recognition of critical aortic stenosis was 82%. Two-dimensional echocardiography is a sensitive method to detect valvular aortic stenosis, and accurately separates patients with aortic stenosis from normal subjects. However, the specificity of 2-D echo in distinguishing critical from noncritical aortic stenosis is limited.

Evaluation of transluminal angioplasty of chronic coronary artery stenosis. Value and limitations assessed in fresh human cadaver hearts.

The possibility of increasing reduced blood flow in atherosclerotic coronary obstruction by catheter balloon dilatation offers a nonsurgical approach to relieve clinical coronary stenosis. To assess the ability of effectively dilating such diseased vessels by transluminal angloplasty, we used the Grlintzig balloontipped catheter in 12 fresh human cadaver hearts in which the intervention was performed in 21 noncalcifled stenotic areas, including each of the three major coronary arteries. Quantitative coronary arteriography documented decreased obstruction of each lesion; luminal diameter increased 58% (1.9 ± 0.2 mm to 2.8 ± 0.3; p < 0.001) and luminal diameter relative to the most proximal normal coronary segment diminished 61% (46 ± 4% to 18 ± 3%; p < 0.001). Angioplasty was most successfully applied in proximal, discrete, noncalcified lesions of the right and left anterior descending coronaries; calcified, tortuous, middle and distal lesions and the left circumflex coronary were entered with difficulty or unapproachable. Histologic examination revealed microanatomic changes, most often endothelial disruption and atheroma compression, but no serious vascular tears. Dilatation beyond normal coronary diameter caused vessel rupture. This study extends elucidation of the value and limitations of percutaneous transduminal angioplasty in the clinical use of this technique in selected patients for relieving coronary obstruction without surgery.

Efficacy of percutaneous transluminal coronary recanalization utilizing streptokinase thrombolysis in patients with acute myocardial infarction

Since coronary thrombosis is a principal factor in the evolving necrotic process in the majority of patients with acute myocardial infarction (AMI), a prospective study was conducted in 25 AMI patients who underwent expeditious coronary arteriography. Of these patients, 22 with totally occluding thrombus also received early streptokinase (STK) administration. STK was given by intracoronary (20 patients) or systemic (two patients) infusion, 2000 to 50,000 IU/min, to a total dose of 125,000 to 500,000 IU within 10 hours of AMI symptom onset. Eighteen patients had angiographically visualized successful coronary thrombolysis; the shorter the interval between onset of symptoms to treatment, the more rapid was the clot dissolution. Successful thrombolysis occurred concomitantly with readily managed reperfusion ventricular tachyarrhythmias in nearly all patients. In addition, STK recanalization resulted in relief of ongoing chest pain in 10 of 12 patients, 10 of 16 evidenced immediate normalization of hyperacute ST segment abnormalities, and 8 of 14 demonstrated subsequent improvement of angiographically visualized left ventricular (LV) ejection fraction. In the percutaneous transluminal coronary recanalization (PTCR) procedure, the step of using a soft-tipped guide wire itself was transiently useful in only one of seven patients in whom this was attempted; reocclusion took place without added STK therapy. Nitroglycerin (NTG) alone produced only slight distal patency in but 1 of 19 patients with coronary occlusion given the nitrate. Importantly, in 14 control AMI patients receiving conventional treatment without STK, 10 showed angiographically complete occlusion of the coronary artery supplying the infarct region 1 month after infarction, thereby excluding spontaneous clot lysis mimicking STK-PTCR-induced reperfusion. These data support the concept that coronary occlusion by thrombosis is inherently involved with AMI and that rapid PTCR application of intracoronary STK provides potent thrombolysis, superior to that provided by NTG and guide wire passage in reestablishing coronary flow with attendant salvage of jeopardized myocardium and with subsequently improved LV function.

Therapeutic efficacy of oral pirbuterol in severe chronic congestive heart failure: Acute hemodynamic and long-term ambulatory evaluation

Abstract Development of effective orally administered cardiotonic agents for sustained ambulatory therapy of severe chronic congestive heart failure (CHF) is currently of considerable clinical interest. Thus we evaluated temporal cardiocirculatory responses to the new ingestible beta-adrenergic receptor agonist pirbuterol (PBL) (0.4 mg/kg) by cardiac catheterization and limb plethysmography in 10 patients with coronary disease and severe CHF refractory to digitalis and diuretics. PBL considerably improved left ventricular (LV) dysfunction during the 6-hour period of hemodynamic monitoring: control lowered cardiac index (CI) of 1.7 L/min/m 2 rose to 2.6 (p 2 (p 2 (p 2 (p 2 (p 0.05) MAP and LVFP, PBL modestly diminished MAP from 83 to 75 mm Hg (p −5 (p −5 (p