ST segment tracking for rapid determination of patency of the infarct-related artery in acute myocardial infarction.

OBJECTIVES: This study was designed to test the hypothesis that monitoring the ST segment on a single electrocardiographic (ECG) lead reflecting activity in the infarct zone provides sensitive and specific recognition of reperfusion within 60 min of initiation of therapy in acute myocardial infarction. BACKGROUND: Infarct-related arteries that fail to recanalize early may benefit from immediate rescue angioplasty. Hence, detection of reperfusion has important practical clinical implications. METHODS: Of 41 patients with acute myocardial infarction who had ambulatory ECG (Holter) monitors placed, 38 had adequate ST segment monitoring for 3 h; 35 of the 38 were treated with thrombolytic agents and 3 with primary angioplasty. All patients underwent early coronary angiography and were classified into two groups: Group P (22 patients) had angiographic patency (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow), the Group O (16 patients) had persistent occlusion (TIMI grade 0 or 1 flow) of the infarct-related vessel at 60 min from initiation of therapy. The initial ST segment level was defined as the first ST segment level recorded; the peak ST segment level was defined as the highest ST segment level measured during the 1st 60 min. To assess the optimal ST segment recovery criteria for reperfusion, the presence or absence of a > or = 75%, > or = 50% and > or = 25% decrement from initial and peak ST segment levels, sampled and analyzed at 2.5-, 5-, 10-, 15-and 20-min intervals, was correlated with patency of the infarct-related artery at 60 min. RESULTS: ST segment recovery of > or = 50% reduction from peak ST segment levels with sampling rates at < or = 10-min intervals provided the optimal criterion for recognizing coronary artery patency at 60 min (sensitivity 96%, 95% confidence interval [CI] 77% to 99%; specificity 94%, 95% CI 69% to 99%, p < 0.0001). The subgroup of 13 patients in Group P with TIMI grade 3 reperfusion flow all met this criterion (sensitivity 100%, 95% CI 75% to 100%). The use of the initial ST segment level as the baseline for determining the presence of a > or = 50% reduction in ST segment levels within 60 min was less sensitive. Prediction of coronary reperfusion within 60 min of therapy on the basis of a > or = 75% decrement from peak ST segment levels was less sensitive, and the use of a > or = 25% decrement was less specific. CONCLUSIONS: ST segment monitoring of a single lead reflecting the infarct zone provides a reliable method for assessing reperfusion within 60 min of acute myocardial infarction. Optimal criteria for ECG reperfusion include a > or = 50% decrease from peak ST segment levels, with ST segment measurements recorded continuously or at least every 10 min.

Randomized placebo-controlled trial of amlodipine in vasospastic angina. Amlodipine Study 160 Group.

OBJECTIVES: This study was designed to assess the efficacy and safety of amlodipine, a long-acting calcium channel blocker, in patients with vasospastic angina. BACKGROUND: Previous studies have established the value of short-acting calcium channel blockers in the treatment of coronary spasm. METHODS: Fifty-two patients with well documented vasospastic angina were entered into the present study. After a single-blind placebo run-in period, patients were randomized (in a double-blind protocol) to receive either amlodipine (10 mg) or placebo every morning for 4 weeks. Twenty-four patients received amlodipine and 28 received placebo. All patients were given diaries in which to record both the frequency, severity, duration and circumstances of anginal episodes and their intake of sublingual nitroglycerin tablets. RESULTS: The rate of anginal episodes decreased significantly (p = 0.009) with amlodipine treatment compared with placebo and the intake of nitroglycerin tablets showed a similar trend. Peripheral edema was the only adverse event seen more frequently in amlodipine-treated patients. No patient was withdrawn from the double-blind phase of the study because of an adverse event. Patients who completed the double-blind phase as responders to amlodipine or as nonresponders to placebo were offered the option of receiving amlodipine in a long-term, open label extension phase. During the extension, the daily dose of amlodipine was adjusted to 5 or 15 mg if needed and the rate of both anginal episodes and nitroglycerin tablet consumption showed statistically significant decreases between baseline and final assessment. CONCLUSION: This study suggests that amlodipine given once daily is efficacious and safe in the treatment of vasospastic angina.

Simultaneous electrical and mechanical alternans in pericardial effusion. Echocardiographic documentation.

A case of pericardial effusion and tamponade with echocardiographic documentation of both electrical and mechanical alternans is described. Alternation of the magnitude of the aortic valve opening reflected the mechanical alternation of the left ventricle. Analysis of the left atrial echoes may provide a possible explanation of the underlying mechanism. The cyclic variations in the magnitude of aortic opening in the weak beats, which are probably respiratory, may represent an echocardiographic counterpart of pulsus paradoxus. Echocardiograms of the aortic root and left atrium in pericardial effusion may help determine the true incidence of simultaneous electrical and mechanical alternans and may have potential value in the diagnosis of cardiac tamponade.

Interim report of multicenter double-blind, placebo-controlled studies of nifedipine in chronic stable angina.

Preliminary results from multicenter double-blind placebo-controlled studies involving crossover and parallel designs were analyzed in 32 and 34 patients with stable angina pectoris entered respectively into the two protocols. The frequency of anginal attacks and the intake of nitroglycerin were decreased about 50 percent in patients receiving nifedipine, and the difference from those on placebo was statistically significant. Similarly, exercise tolerance was significantly increased with nifedipine, as evidenced by several variables, and the degree of ischemia was believed decreased, as reflected by lesser ST segment depression at peak exercise. The heart rate-blood pressure product, an approximation of myocardial oxygen consumption, was slightly but significantly decreased at equivalent workloads, but was not significantly different from placebo at the onset of angina or at maximal exercise. Adverse reactions to nifedipine, although frequent, were generally benign and usually responded to dose adjustment or improved spontaneously. These results suggest that the calcium antagonist nifedipine is effective and safe in the treatment of chronic stable angina.

Comparison of cold pressor and exercise radionuclide angiocardiography in coronary artery disease.

To investigate the role of the cold pressor test (CPT) with radionuclide angiocardiography in the diagnosis of coronary artery disease (CAD), we performed angiocardiography in 52 patients (18 with angiographically normal coronary arteries and 34 with CAD) during the resting state, CPT, and supine bicycle exercise (EX). In normal subjects, left ventricular ejection fraction (EF) was unchanged between rest (58 +/- 9%) and CPT (59 +/- 9%, p = ns), but increased during maximal EX (69 +/- 9%, p less than 0.01). In CAD patients, EF fell from 55 +/- 9% at rest to 49 +/- 9% during CPT (p less than 0.01), and to 53 +/- 11% during EX (p = ns vs. rest). Twenty-seven CAD patients (79%) developed new or worsening areas of dyssynergy during CPT, vs. 25 patients (73%) during EX. Thus, the cold pressor test with radiocardiography appears to be a useful noninvasive test for the diagnosis and functional evaluation of CAD, particularly in patients unable to perform a satisfactory exercise test.

Effect of nifedipine on exercise-induced left ventricular dysfunction and myocardial hypoperfusion in stable angina.

To assess the effects of nifedipine on left ventricular function and regional myocardial perfusion, exercise radionuclide ventriculography was performed in 15 men (median age 59 years) and exercise thallium-201 scintigraphy was done in 11 of them, before and 90 minutes after the oral administration of 20 mg of nifedipine. All patients had stable angina and angiographically proved coronary artery disease without evidence of spasm. Exercise tolerance after administration of nifedipine increased from 343 +/- 42 seconds to 471 +/- 50 seconds (p less than 0.01), whereas the peak exercise double product remained essentially unchanged (difference not significant). Ejection fraction improved significantly at rest (from 49 +/- 3.6% to 52 +/- 3.3%, p less than 0.05) and at peak exercise (42 +/0 3.3% to 47 +/- 3.7%, p less than 0.05). Nifedipine also resulted in an improved segmental wall motion score (4.3 +/- 2.3 to 3.0 +/- 2.3, p less than 0.05; 0 = normal and 4 = worst degree of dysfunction). The ejection fraction increased by more than 5% in one third of the patients at rest, and in more than half of the patients at peak exercise. Improved exercise myocardial perfusion occurred in 5 of 11 patients (45%) and in 7 of 28 segments (25%) with reversible hypoperfusion. Thus, nifedipine produces significant improvement in global and regional left ventricular function in patients with coronary artery disease and stable angina. This may be accounted for, at least in part, by improvement in myocardial perfusion.

Exercise-induced coronary arterial spasm: angiographic demonstration, documentation of ischemia by myocardial scintigraphy and results of pharmacologic intervention.

Exercise-induced coronary arterial spasm is an infrequently recognized phemonemon whose mechanism and management are not well established. In two patients with reproducible exercise-induced S-T segment elevation and angina pectoris thallium-201 scintigraphy showed areas of reversible anteroapical hypoperfusion, and gated radionuclide ventriculography revealed anteroapical hypokinesia with a decrease in left ventricular ejection fraction at peak exercise. During coronary arteriography supine exercise provoked occlusive spasm of the left anterior descending coronary artery, which at rest had only minimal plaques. Consequently, treadmill testing was performed with five different pharmacologically provoked interventions: direct vasodilatation (nitrates), alpha adrenergic blockade (phenmoxybenzamine), beta adrenergic blockade (propranolol), calcium flux blockade (verapamil), and prostaglandin inhibition (indomethacin). Exercise-induced coronary arterial spasm, manifested as S-T segment elevation and angina, was prevented by nitrates, but was not eliminated by short-term oral administration of an alpha or beta blocking agent, a calcium antagonist or a prostaglandin inhibitor. Further, beta adrenergic blockade appeared to be detrimental. Thus, this study demonstrates (1) that coronary arterial spasm may be the underlying mechanism of at least some cases of exertional angina associated with transient perfusion deficits and left ventricular dysfunction, and (2) that it may be prevented by oral nitrates.

Cardiac arrhythmias associated with prophylactic pacing during coronary angiography.

Data from 518 consecutive cardiac catheterizations were analyzed to test the value of prophylactic pacemaker insertion during coronary angiography and to compare the incidence of arrhythmic complications in patients with and without pacemakers. In patients without pacing (n = 273), 1 episode of ventricular fibrillation occurred, which responded promptly to defibrillation. Sinus bradycardia (fewer than 30 beats/min for 10 seconds) was recorded in 74 patients (27%) and required treatment in 30 (11%). No patient required or would have benefited from pacemaker placement. Of the 245 patients with prophylactic pacemakers, there was an increased incidence of all ventricular (9 vs 1; p less than 0.013) and supraventricular (5 vs 0; p less than 0.046) arrhythmias. Pacemaker-associated induction of ventricular fibrillation occurred in 2 patients and was clearly related to electrical stimulation during a normally non-vulnerable period of the cardiac cycle. In conclusion, routine prophylactic pacemaker insertion during coronary angiography is not warranted in patients with normal sinus rhythm and normal atrioventricular conduction. More information is needed to determine if pacing is needed in patients with conduction system disease.

Acute ventricular septal rupture. Angiographic-morphologic features and clinical assessment.

Twenty patients with acute ventricular septal rupture underwent cardiac catheterization. Prior to catheterization, 17 patients were in Killip class 3-4. Mean cardiac index and cardiac output were 2.03 +/- 0.81 L/min/m2 and 3.55 +/- 1.33 L/min, respectively. Based on a recent pathologic description of septal rupture, we encountered by angiography and during surgery, two morphologic types of rupture: simple type which appears as a direct through-and-through communication between the ventricles, and complex type which presents hemorrhagic tracts in the septum with the opening into the ventricles at different levels. Considering the management of patients with septal rupture and the clinical outcome in our series, it is suggested that there is a need to minimize invasive angiographic procedures prior to early surgical correction of the ruptured septum.

The mechanism of hypotension following angiography.

The hypotension observed following the intracardiac injection of contrast media is believed to be the result of myocardial depression, peripheral vasodilatation, or both. It is unclear which of these factors is primarily involved in different types of angiography. To assess this problem, Renografin-76 was injected into the aortic root of 15 anesthetized dogs (1 ml/kg) and into the left coronary artery (3-5 ml) in 18 dogs. The heart rate, the systolic and diastolic arterial pressures, left ventricular pressure, peak dp/dt and dp/dt-40 were monitored continuously until return to baseline. Following selective left coronary artery injection, both systolic and diastolic pressures decreased maximally at 5 seconds with parallel changes in peak dp/dt and dp/dt-40. Following the aortic root injection, the blood pressure response was biphasic, increasing at 5 seconds and decreasing maximally at 20 seconds. The corresponding changes in peak dp/dt and dp/dt-40 were initial depression at 5 seconds with quick return to baseline and increase above control at the time of maximal hypotension. The left ventricular end diastolic pressure rose maximally at 5 to 10 seconds for both coronary and aortic injections. The mechanism of hypotension, therefore, varies with the type of angiography. Myocardial depression appears to be a primary factor with selective coronary angiography. However, with aortic root injection, myocardial contractility, although initially depressed, is already improved at the time of maximal hypotension, and thus peripheral vasocilatation is probably the prime mechanism of the hypotension.

The diagnosis of coronary artery spasm in the cardiac catheterization laboratory.

Coronary artery spasm can now be well documented in the cardiac catheterization laboratory. At present, reliable criteria are available for the diagnosis of severe episodes that are characteristic of patients with Prinzmetal's variant angina. Newer criteria for the diagnosis of milder episodes of spasm are gradually being developed. Optimal criteria may become available with further progress of quantitative angiography. Provocation techniques for the induction of an attack of spasm in the cardiac catheterization laboratory are widely available. Of these, ergonovine testing is the most popular. The tests can usually be performed by experienced angiographers with impressive safety and provide a high degree of sensitivity and specificity when used in patients with the clinical diagnosis of variant angina. Although the research applications of such techniques are extremely broad, their practical clinical indications are somewhat limited to the work-up of patients with infrequent chest pains and normal or near-normal coronary arteriograms. There are other indirect methods for the diagnosis of coronary spasm, but the ideal technique is not available yet. Further expansion of newer modalities for the diagnosis of coronary artery spasm will certainly enhance our understanding of myocardial ischemia and will improve our ability to manage patients with ischemic heart disease.

Lead systems: sensitivity and specificity.

In this article, the modified 12-lead system and the bipolar lead systems are discussed, both of which may provide adequate sensitivity and specificity of stress tests for clinical purposes. A single lead V5 or, preferably, bipolar modification of lead V5 may be adequate in certain situations in which cost or the type of population being tested legitimizes such a choice. However, the modified 12-lead system is far more popular for the diagnosis and follow-up of patients with ischemic heart disease. The final choice of lead system for monitoring stress tests will ultimately depend on the needs and resources of a given laboratory.

Anomalous coronary arteries: angiographic findings in 80 patients.

Among 13010 adults who underwent coronary arteriography, 80 (0.61%) patients had a total of 83 anomalous coronary arteries. Thirty-three (41%) of the patients were of Hispanic origin, while out of the entire population studied 30% were Hispanic. The right coronary artery was the most common anomalous vessel. It was identified in 50 (62%) patients, arising in 35 from the left aortic sinus, in 14 from the posterior sinus, and in 1 from the left coronary artery. An anomalous circumflex artery was recognized in 22 (27%) patients. Nine (11%) patients presented an anomalous left anterior descending artery, 1 patient an anomalous left main coronary artery, and another an anomalous septal perforator artery. Twenty-three (29%) patients had concomitant congenital heart abnormalities, most commonly. bicuspid aortic valve and mitral valve prolapse. In each of 5 patients with complex congenital heart disease the course of the anomalous vessel could have interfered with a surgical procedure. In 4 cases anomalous coronary arteries were associated with either anomalous systemic venous circulation or anomalous cardiac veins. In 5 (6%) patients only, the anomalous coronary artery was solely responsible for a clinical event. Coronary atherosclerosis of the anomalous arteries was found in 28% of the patients, while the overall incidence of the disease in this series was 65%. Thus, anomalous coronary arteries are associated with a high incidence of congenital heart diseases, but do not appear to be associated with an increased risk for development of coronary atherosclerosis. The angiographic recognition of these vessels is important in patients who undergo coronary angioplasty or cardiac surgery. Variations in the frequency of congenital coronary anomalies as reported herein may be attributed to a genetic background.

Effects of digoxin on left ventricular function in coronary artery disease patients.

To assess whether digitalis modifies or prevents the deterioration of the left ventricular ejection fraction and wall motion during acute ischemia, we performed gated blood pool radionuclide ventriculograms in 15 patients with angiographically documented coronary artery disease. All patients were studied in the resting state and during maximal supine bicycle exercise, both before and 1 hour after 1 mg intravenous digoxin. There was no significant difference, pre-digoxin vs post-digoxin, in exercise tolerance (415 +/- 84 vs 418 +/- 107 seconds), number of segments with abnormal resting wall motion (12 vs 11) or exercise wall motion (21 vs 19). Ten patients developed angina during the same exercise load, irrespective of digoxin administration. Twelve patients had subnormal left ventricular ejection fraction during exercise pre-digoxin, vs 13 patients post-digoxin (P = ns). In the resting state, the left ventricular ejection fraction was higher after digoxin (53 +/- 14% pre vs 58 +/- 14% post, P less than 0.05). During exercise, however, the left ventricular ejection fraction was not significantly improved after digoxin (50 +/- 16% pre vs 53 +/- 17% post, P = ns). These data indicate that although acute administration of digoxin improves the resting left ventricular function, it does not improve exercise tolerance to angina. Furthermore, intravenous digoxin does not appear to prevent the deterioration of left ventricular wall motion and ejection fraction during exercise induced ischemia.

Coronary artery spasm: its role in the pathogenesis of myocardial ischemia.

The role of coronary artery spasm in the production of myocardial ischemia has recently become the focus of increased attention. This phenomenon is now well established as a causative mechanism underlying the resting chest pain attacks in Prinzmetal's variant angina. There is also evidence that coronary spasm may play a more significant role in the broad spectrum of ischemic heart disease than can be documented by current techniques. The autonomous nervous system constitutes a major element in the pathophysiology of spasm. Coronary arteriography, in spite of important limitations, remains the only technique for final documentation of this phenomenon, but radionuclide scintigraphy appears to be promising. Nitroglycerin is effective for the relief of the acute attack, while long acting nitrates and the calcium antagonists: nifedipine, perhexiline and verapamil are useful in the prevention of recurrences.

Isolated left posterior fascicular block associated with acquired ventricular septal defect.

Isolated left posterior fascicular block in the absence of associated right bundle-branch block is a rare electrocardiographic finding. In view of its anatomy and the fact that it receives a dual blood supply, the posterior fascicle of the left bundle branch appears to be less vulnerable than the anterior fascicle or the right bundle. Mechanical disruption of the posterior fascicle can produce isolated left posterior fascicular block. This has been demonstrated in animal models. However, such occurrence has not been noted in humans. We present two cases of inferior wall myocardial infarction, complicated by rupture of the inferior septum, resulting in isolated left posterior fascicular block. The development of isolated left posterior fascicular block complicating myocardial infarction may, therefore, serve to alert to the possible underlying septal rupture.

The magnitude of exercise-induced ST segment depression and the predictive value of exercise testing.

The assess whether the magnitude of exercise induced ST segment depression improves the predictive values of symptom limited exercise tests, and helps in the recognition of patients with more severe coronary heart disease, 90 consecutive patients with positive treadmill tests who also underwent selective coronary arteriography were reviewed. The predictive value improved progressively with the increasing ST depression and was most reliable in a select group of patients with normal electrocardiographic baseline who were not receiving digitalis (73% with ST depression greater than or equal to 1 mm to 100% with ST depression greater than or equal to 4 mm). The incidence of 2 and 3 vessel disease increased from 61% with ST depression greater than or equal to 1 mm in the overall population to 100% with ST depression greater than or equal to 4 mm in the select group, and the incidence of left main trunk lesions increased, respectively from 6 to 30%. The prediction of 2 and 3 vessels disease was found to be significantly greater when patients were dichotomized into those with ST depression greater than or equal to 4 mm compared to less than 4 mm. It is concluded that the magnitude of ST segment depression definitely improves the predictive values of exercise tests as well as the ability to recognize the patients with more severe disease. However, the markedly positive exercise tests cannot be utilized to accurately predict the presence of 2 or 3 vessel disease in individual cases unless ST depression attains 4 mm or more in patients with normal electrocardiographic baseline who are not taking digitalis. In this group, the ability to predict left main trunk lesion is approximately 30%.

Diastolic mitral regurgitation in patients with hypertrophic cardiomyopathy.

An analysis of the left ventricular angiograms of 31 patients with hypertrophic cardiomyopathy revealed diastolic mitral regurgitation in 4, a prevalence of 12.9%. The clinical, echocardiographic, angiographic, and hemodynamic data of these patients were reviewed. Diastolic mitral regurgitation could not be attributed to arrhythmia, PR interval prolongation, atrioventricular dissociation, aortic insufficiency, or aortic stenosis. Reduced left ventricular compliance was evidenced by elevated end-diastolic pressure following angiography and reduced diastolic E-F slope on echocardiography. It is speculated that the rapid inflow of blood into a poorly compliant ventricle established a turbulent flow pattern that resulted in the "floating" of blood back into the left atrium.

Coronary artery spasm. What is its role in ischemic heart disease?

Knowledge of the pathophysiology of myocardial ischemia has been greatly enhanced recently by new information on coronary artery spasm. This phenomenon accounts for the mechanism underlying the attacks of resting chest pain in Prinzmetal's angina and plays a role in almost all aspects of ischemic heart disease. The diagnosis of coronary artery spasm can be made presumptively with noninvasive methods, but definitive documentation is usually obtained in the cardiac catheterization laboratory. The nitrate derivatives and the calcium antagonists provide a safe and effective approach to therapy.