Augusto D. Pichard

Septal perforator compression (Narrowing) in idiopathic hypertrophic subaortic stenosis

Thirteen patients with idiopathic hypertrophic subaortic stenosis were compared with two groups of subjects: 10 patients with chest pain, normal coronary arteries and a normal left ventricle, and 10 patients with left ventricular hypertrophy. Five of the latter had aortic stenosis and five had idiopathic left ventricular hypertrophy. Coronary arteriography revealed that the septal branches of the left anterior descending artery closed or narrowed during systole in patients with idiopathic hypertrophic subaortic stenosis and did not do so in the other patient groups. This narrowing is possibly related to an abnormal position of the septal arteries within the septum in idiopathic hypertrophic subaortic stenosis. Systolic compression of the septal perforator arteries is not a pathognomonic sign of idiopathic hypertrophic subaortic stenosis.

Spectrum of exercise thallium-201 myocardial perfusion imaging in patients with chest pain and normal coronary angiograms.

Abstract Twenty-seven consecutive patients with chest pain and no significant obstructive coronary lesions on arteriography were studied with thallium-201 myocardial imaging during exercise and at rest. Fifteen of the patients had typical and 12 atypical angina pectoris. All underwent treadmill exercise electrocardiographic testing; the results were abnormal in 10 patients (37 percent), normal in 14 (52 percent) and uninterpretable in 3 (11 percent). The exercise and resting thallium-201 myocardial images were normal in 23 patients (85 percent); the results of exercise testing were normal in 12 of these patients, abnormal in 8 and uninterpretable in 3. Four patients had a perfusion defect on exercise thallium-201 myocardial imaging; the defect filled in by 4 hours in two patients but persisted in the other two. In contrast, when thallium-201 myocardial imaging was performed in 28 consecutive patients with angiographic coronary artery disease, only 5 patients (16 percent) had normal exercise and resting thallium-201 myocardial images. Therefore, thallium-201 myocardial imaging offers a more effective means of identifying patients with chest pain and no obstructive coronary artery disease than the clinical history or the exercise electrocardiographic test, or both. However, 15 percent of these patients will have abnormal exercise thallium-201 myocardial images because of factors that have not yet been identified.

Acute coronary hemodynamic response to cigarette smoking in patients with coronary artery disease

The acute changes in coronary blood flow and coronary resistance that occur in response to cigarette smoking have not been accurately determined. To define the factors that affect this response, coronary sinus blood flow was measured in 16 patients (group I) with coronary artery disease and in 6 patients (group II) without angiographically detectable coronary disease. Seven patients (group IA) had severe (greater than or equal to 75%) proximal left coronary lesions and nine patients (group IB) had significant distal lesions with 50% or less proximal stenoses. Group I had a smaller overall increase (increases 1.6 +/- 5.3%) in coronary sinus blood flow than did group II (increases 7.7 +/- 6.1%) (p less than 0.05). Coronary resistance increased overall (increases 2.7 +/- 5.3%) in group I but decreased (decreases 2.4 +/- 3.4%) in group II (p less than 0.05). Patients in group IA had a highly significant increase in coronary resistance as compared with group IB (increases 7.0 +/- 4.2% versus decreases 0.9 +/- 2.6%) (p less than 0.001). Coronary sinus flow tended to decrease (decreases 1.2 +/- 4.6%) in group IA but to increase (increases 3.8 +/- 5.1%) in group IB (p = 0.06). It is concluded that smoking increases coronary resistance in patients with coronary artery disease. A greater impact is observed in patients with a severe proximal stenosis than in those with a distal stenosis. It is proposed that smoking increases coronary artery tone at the site of the stenosis, limiting the coronary flow response proportionally to the size of the affected vascular bed.

Can noninvasive exercise test criteria identify patients with left main or 3-vessel coronary disease after a first myocardial infarction?*

This study attempts to determine whether exercise treadmill testing with clinical, electrocardiographic, and thallium-201 myocardial perfusion imaging data can identify which patients have left main or 3-vessel (anatomically high-risk) coronary artery disease (CAD) after their first transmural myocardial infarct (MI). Twelve exercise test criteria for high-risk disease were compared in 40 patients referred for cardiac catheterization; 34 had a history of chest pain and 17 had angiographically defined high-risk CAD. A thallium image defect outside the vascular distribution of the MI was the most reliable criterion to distinguish patients with high-risk CAD (p = 0.00052 for Fishers exact test of discrimination). Thallium imaging was somewhat more sensitive (92 versus 65%, p = 0.108) when patients with negative thallium imaging criteria who failed to achieve 85% of the age-predicted maximal heart rate were excluded. Failure to achieve 85% of predicted heart rate was by itself a useful criterion for detecting high-risk CAD (p = 0.017), especially in patients not taking propranolol (p = 0.004). Development of positive S-T segment depression at less than 70% predicted heart rate also discriminated left main or 3-vessel disease from less extensive CAD (p = 0.016). Other criteria failed to discriminate significantly between high-risk and less extensive CAD in patients after their first MI (p greater than 0.05). S-T segment depression (p = 0.199) or chest pain (p = 0.577) during exercise testing were particularly unreliable. Further, none of the criteria for high-risk CAD were influenced by irreversible left ventricular dysfunction. It is concluded that patients with thallium imaging defects outside the region of the infarct, decreasing blood pressure during exercise, failure to achieve 85% of predicted heart rate, or S-T depression at less than 70% of predicted heart rate have a high probability of having left main or 3-vessel disease. Patients without these criteria have a very low probability of having high-risk CAD and probably do not need coronary angiography for the purpose of excluding these high-risk coronary lesions after a first MI.

Large V waves in the pulmonary wedge pressure tracing in the absence of mitral regurgitation.

Abstract The accurate diagnosis of mitral regurgitation has important therapeutic implications. We have observed that large V waves in the pulmonary wedge pressure (PW) may be misleading In the diagnosis of mitral regurgitation. Of 237 consecutive patients with high quality hemodynamic, angiographic, and echocardiographic data, 27 had large V waves (peak V 10 mm Hg greater than pulmonary wedge mean pressure). Ventriculograms were analyzed in blind fashion by 3 expert angiographers for any angiographic evidence of mitral regurgitation; 17 patients had mitral regurgitation (group I), and 10 did not (group II). The control group (group III) of 22 patients had normal V waves and no mitral regurgitation. Twenty-two hemodynamic and echocardiographic variables were compared among groups. The only significant difference between groups I and II was in the slope of the ascent of the V wave (74.3 versus 141.9 mm/s, p=0.021), also expressed as the mitral regurgitation index (6.01 versus 9.45, p=0.005). A slope of 100 mm/s or slower had a sensitivity of 80% to confirm mitral regurgitation and a specificity of 70% to rule it out. The size of the V wave and the VPW mean ratio were similar in groups I and II (38.5 ± 11 versus 37.5 ± 11 mm Hg, and 1.67 ± 0.3 versus 1.69 ± 0.4, respectively, mp=NS) and were not helpful in predicting the presence or absence of mitral regurgitation. Among patients without mitral regurgitation (groups II and III), those with large V waves had a higher pulmonary wedge mean pressure (23.5 versus 15.6 mm Hg, p = 0.01), a higher A wave (25.3 versus 16.4 mm Hg, p = 0.032), a more elevated mitral regurgitation index (9.45 versus 3.99, p = 0.001), a larger left atrial size (24.5 versus 21.6 cc, p = 0.05), a greater V wave to pulmonary wedge mean pressure ratio (1.69 versus 1.10, p = 0.001), and a faster slope of ascent of the V wave (141.9 versus 53.05 mm/s, p = 0.005). We conclude that large V waves in the pulmonary wedge pressure tracing can be seen in the absence of mitral regurgitation. The size of the V wave is related to factors that determine left atrial compliance. Caution is called for in the diagnosis of mitral regurgitation by pulmonary wedge pressure alone.

Silent ST segment deviations and extent of coronary artery disease

Fifty patients who underwent coronary and left ventricular angiography for suspected coronary artery disease (CAD) had ambulatory ECG monitoring at a time remote from that of catheterization. After correcting for positional ST segment variation on ambulatory ECG, the amount of time that ST segments deviated more than 1 mm. from baseline without corresponding angina was determined, and these results were correlated with results of angiography. Silent ST segment deviations were seen in patients without significant CAD in 2.2% of observations, but increased significantly with extent of coronary artery disease (2.9%, 8.2%, and 10.1% of observations in the one-, two-, and three-vessel disease groups, respectively). This relationship was independent of ventricular function, resting ECG, and previous symptoms. It is concluded that silent ST segment deviations on ambulatory ECG reflect the presence and severity of coronary artery disease.

Effects of Chronic Tobacco Smoking on the Coronary Circulation

The effects of chronic smoking on the coronary circulation were studied by evaluating the coronary vascular reserve in 12 chronic smokers (group 1) and 10 nonsmokers (group 2). All patients were referred to cardiac catheterization for evaluation of chest pain and were found to have normal coronary and left ventricular angiograms. Coronary vascular reserve was measured by analyzing the hyperemic response to selective coronary injection of contrast agent. There was no statistically significant difference between groups 1 and 2 with regard to age, baseline electrocardiogram or response to treadmill or thallium-201 exercise tests. The mean coronary reserve (+/- standard deviation) was 74.1 +/- 20.1% in the smokers versus 117.1 +/- 45.1% in the nonsmokers (p less than 0.02). In patients who smoked 1 pack a day or less and in those who smoked more than 1 pack a day, the mean coronary reserve was 89.5 and 64.9%, respectively (p less than 0.05). Additionally, of 20 patients followed up for an average of 20 months, 7 of 10 smokers and 1 of 10 nonsmokers continued to have chest pain (p less than 0.03). The cause for the chest pain has not been established in these patients. These results suggest that coronary vascular reserve is significantly less in chronic smokers than in nonsmokers, and that this decrease is more pronounced in heavy smokers.

Abnormal regional myocardial flow in myocardial bridging of the left anterior descending coronary artery

A patient with angina pectoris, myocardial bridging of the left anterior descending coronary artery and otherwise normal coronary arteries is presented. Regional myocardial blood flow was studied with the thermodilution technique. Atrial pacing of the heart at a rate of over 140/min reproduced the anginal syndrome, with S-T segment depression in the electrocardiogram. There was a transient decrease in great cardiac vein flow during rapid pacing with a simultaneous increase in total coronary sinus flow. The study demonstrates that in this patient, a myocardial bridge was associated with decreased blood flow to the area perfused by the bridged artery with a concomitant increase in coronary sinus flow as the pacing rate was increased from 96 to 150 and 180/min. After administration of nitroglycerin, the bridging effect was more accentuated on angiography; pacing-induced tachycardia was associated with similar changes in great cardiac vein and coronary sinus flows with less S-T segment depression in the electrocardiogram and chest pain of milder intensity.

Determinants of ventricular tachycardia in patients with coronary artery disease and ventricular aneurysm: Clinical, hemodynamic, and angiographic factors

Many patients with coronary artery disease (CAD) in whom ventricular tachycardia (VT) develops have transmural scars or frank aneurysms. However, only a minority of patients with ventricular aneurysms go on to develop VT. To determine which factors are associated with the development of VT in patients with aneurysms, we retrospectively reviewed the records of 154 patients with CAD and segments of akinesia or dyskinesia, or both, on left ventriculography. Of the 154 patients, 85 had 24-hour Holter monitoring or 48 consecutive hours of continuous electrocardiographic monitoring in an intensive care unit within 6 months of catheterization. VT occurring at least 10 days after myocardial infarction (MI) or in the chronic phase was recorded in 19 patients (Group I); the remaining 66 patients did not have VT (Group II). The clinical, hemodynamic, and angiographic characteristics of these 2 groups showed no significant difference with respect to age, time from first transmural MI to catheterization, congestive heart failure (CHF), ejection fraction, or presence of dyskinesia. Patients with VT had significantly larger aneurysms and a higher prevalence of septal akinesia or dyskinesia. However, stepwise discriminant analysis revealed septal akinesia or dyskinesia to be the only independently significant variable distinguishing the 2 groups. Thus, septal involvement appears to be a major determinant of VT in patients with CAD and ventricular aneurysm.

Angiographic study of the infarct-related coronary artery in the chronic stage of acute myocardial infarction

We and others have demonstrated a high prevalence of total coronary occlusion during the acute phase of myocardial infarction (MI). This study reports the angiographic appearance of the infarct-related artery (IRA) in 130 patients with a history of MI, who underwent cardiac catheterization 2 weeks to more than 12 months afterwards. The IRA was the left anterior descending in 47%, the right coronary artery in 50%, and the circumflex in 3% of cases. Total coronary occlusion was found in 80% of patients studied 2 to 4 weeks after MI, and decreased gradually reaching 40% of those studied after 12 months of MI. In those patients with a patent IRA, severe stenosis remained: 99% obstruction at 2 to 4 weeks, decreasing to 85.9% obstruction after 12 months (p less than 0.005). The prevalence of total coronary occlusion (TCO) and the severity of stenosis in those without TCO was similar in those with transmural or nontransmural MI and in those with one-, two- or three-vessel disease. This study suggests that endogenous lysis is probably a slow process, and that severe coronary narrowing persists in those with recanalization.