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Vectorcardiograms (VCG) from a consecutive group of 77 patients with significant aortic valve disease were analyzed. All of the patients had complete left and right heart catheterization with normal coronary arteriograms and normal left ventricular contraction. Thirty-five (46%) patients met VCG criteria for anterior myocardial infarction (AMI-35%) and/or inferior myocardial infarction (IMI-14%). This was a significant increase in false positive diagnosis for both criteria compared to a group of 200 normal volunteers under age 30 and 100 patients with normal hearts by cardiac catheterization (P less than 0.01). It was found that if the VCG diagnosis of myocardial infarction was deferred when the maximal transverse plane magnitude was greater than 1.9 mV, the incidence of AMI false positive diagnosis decreased to 3% and the incidence of IMI false positive diagnosis decreased to 1%. The same rule was applied to the aortic valve disease cohort, a group of 124 patients with documented AMI and a group of 158 patients with IMI. This decreased the sensitivity of the AMI criteria from 93 to 83% and of the IMI criteria from 85 to 77%. The increase in average performance was statistically significant fro the AMI criteria (P less than 0.05) but not for the IMI criteria.

These studies were designed to define the effect of atrial natriuretic peptide (ANP) on coronary flow. ANP was infused as a bolus directly into the left circumflex coronary artery in doses ranging from 0.05 to 5 micrograms in nine open-chest, anesthetized dogs. Coronary flow was measured with an electromagnetic flowmeter. Regional transmural myocardial blood flow and distribution were measured with 11.3 +/- 0.25 micron radionuclide-labeled microspheres. No significant change was noted in systemic hemodynamics (heart rate, arterial pressure, left atrial pressure, or cardiac output) during the course of the studies. ANP produced a transient vasodilatation of coronary resistance vessels and increased flow by 41% after both the 2.5 and 5 micrograms doses. The vasodilatation occurred uniformly throughout the ventricular wall so that the endocardial/epicardial flow ratio remained constant. There was no evidence of coronary vasoconstriction. The peak vasodilatation response occurred 28 +/- 7 sec after the beginning of the infusion of ANP and lasted approximately 3 min. These data support the hypothesis that ANP administration is associated with a vasodilator response in the coronary resistance vessels that may be modulated through either the release of another vasodilator substance or another mechanism.

Frank-lead vectorcardiograms (VCGs) and standard 12-lead electrocardiograms (ECGs) were analyzed to develop simple, linear, quantitative criteria for the diagnosis of right ventricular hypertrophy (RVH). The study subjects included a population with a definite RVH (84 patients with mitral stenosis proved by cardiac catheterization and pulmonary arterial systolic pressure > 40 mm Hg) and a population with minimal likelihood of RVH (173 young, healthy volunteers and 151 normal subjects proved by cardiac catheterization). VCGs were evaluated to identify criteria that provided maximum sensitivity and at least a 95% specificity: the maximum QRS magnitude had to be < 1.8 mV and either (1) the amplitude at -45 degrees (transverse plane) had to be < 0.3 mV or (2) the maximum anterior amplitude plus the maximum rightward amplitude minus the amplitude at -45 degrees must be greater than or equal to 0.5 mV. Application of these criteria achieved 60% (50 of 84) sensitivity in patients with RVH, similar to that for previous VCG criteria but significantly better (p < 0.01) than the best sensitivity with any ECG criteria (27%, 23 of 84). The specificity of the proposed criteria was 96% (310 of 324), significantly better (p < 0.001) than the 78% specificity (252 of 324) of existing VCG criteria. Thus, linear measurements of the QRS complex displayed on the VCG identify 60% of patients with moderate-to-severe RVH and falsely indicate RVH in only 4% of normal subjects.

Function of the coronary collateral circulation during the course of a single abrupt coronary occlusion was evaluated in awake dogs instrumented over the long term. Studies were performed approximately 2 weeks after collateral development had been stimulated in the dogs by partial stenosis of the proximal left circumflex coronary artery. The pressure drop from the central aorta to the distal circumflex coronary artery was measured continuously. Under control conditions and at 30 sec and 4 min of a single abrupt complete circumflex occlusion, myocardial blood flow was determined by a radioactive microsphere technique. Coronary collateral conductance was calculated as mean collateral blood flow divided by the mean drop in pressure. The following was noted in dogs that developed collateral vessels: during the coronary occlusion, mean distal circumflex coronary pressure increased from 42 +/- 9 to 49 +/- 10 mm Hg (p less than or equal to .01); mean collateral flow increased from 0.78 +/- 0.30 to 0.84 +/- 0.33 ml/min/g (p less than or equal to .05); the endocardial/epicardial flow ratio increased from 0.77 +/- 0.36 to 1.04 +/- 0.25 (p less than or equal to .01); and the coronary collateral conductance increased significantly from 0.017 +/- 0.017 to 0.021 +/- 0.021 (ml/min/g)/mm Hg (p less than or equal to .005). These data suggest that during a brief occlusion of a major coronary artery, immature coronary collateral channels do not reach maximal function immediately after the occlusion. Rather, coronary collateral conductance increases with time and may be associated with improved transmural perfusion of the myocardium.