The effects of pretreatment with nitroglycerin on ischemic left ventricular dysfunction during coronary angioplasty.

To evaluate the degree to which nitroglycerin reduces myocardial ischemia and dysfunction induced by transient coronary occlusion, 19 patients were studied during coronary angioplasty of the left anterior descending coronary artery. After a control occlusion of 60 seconds, 0.2 mg nitroglycerin was administered intravenously and the occlusion was repeated for 60 seconds. Before and during the occlusion period, pulmonary capillary wedge pressure was measured, the intracoronary ECG was recorded, and ventricular volumes, ejection fraction, and regional systolic shortening were obtained by digital subtraction angiography. Nitroglycerin caused a significant fall in pulmonary capillary wedge pressure before (10 vs. 7 mmHg) and at 60 seconds occlusion (18 vs. 14 mmHg), but did not significantly delay the rise in wedge pressure (37 vs. 44 seconds). End-systolic left ventricular volume at 60 seconds of occlusion was reduced by nitroglycerin (77 vs. 68 ml), whereas regional shortening of the ischemic segments remained unchanged (22 vs. 23%). Nitroglycerin did not delay the onset of ischemic ST-segment elevation (14 vs. 14 seconds) and had no effect on the changes of ST elevation in the intracoronary ECG (1.9 vs. 1.9 mV). These findings suggest that intravenous nitroglycerin reduces filling pressure and slightly improves left ventricular global function during acute coronary occlusion. Nitroglycerin, however, has little effect on ischemia-induced regional dysfunction and on ST-segment elevation in the intracoronary ECG.

Protective effects of pretreatment with intracoronary nifedipine on myocardial ischemia and dysfunction.

To assess whether pretreatment with intracoronary nifedipine protects the myocardium against acute ischemia induced by coronary occlusion, 18 patients were studied during coronary angioplasty of the left anterior coronary artery. After a control occlusion of 60 seconds, 0.1 mg nifedipine was injected and occlusion was repeated for 60 seconds. Before and during the occlusion period, pulmonary capillary pressure was measured and the intracoronary epicardial ECG was recorded. After intracoronary administration of nifedipine, the onset of the rise in diastolic filling pressure was delayed from 23 to 38 seconds (p less than 0.01) and the changes at 60 seconds of occlusion were reduced from 14 to 11 mmHg (p less than 0.05). Nifedipine delayed the appearance of ischemic ST-segment elevation in the intracoronary ECG from 11 to 21 seconds (p less than 0.01) and diminished the changes at 60 seconds of occlusion from 1.8 to 1.2 mV (p less than 0.05). These findings suggest that pretreatment with intracoronary nifedipine protects the myocardium against some of the mechanical and electrocardiographic consequences of regional ischemia during acute coronary occlusion.

Heparin and infarct coronary artery patency after streptokinase in acute myocardial infarction.

Anticoagulant therapy is frequently used after thrombolytic agents in the treatment of acute myocardial infarction (AMI) although it is unclear that such therapy will prevent subsequent infarct vessel reocclusion. The role of duration of heparin therapy in maintaining infarct artery patency was studied retrospectively in 53 consecutive AMI patients who received streptokinase therapy and underwent coronary angiography acutely and at 14 +/- 1 days. Of the 39 patients with initial infarct vessel patency, patency at follow-up angiography was observed in 100% (22 of 22) of those who received greater than or equal to 4 days of intravenous heparin but in only 59% (10 of 17) of those patients who received less than 4 days of heparin (p less than 0.05). Of the 14 patients not initially recanalized after streptokinase, patent infarct-related arteries at follow-up angiography were found in 3 of 8 (38%) treated with greater than or equal to 4 days of heparin therapy but in none of the 6 patients treated for less than 4 days (difference not significant). No significant difference in hemorrhagic complications was noted between the short- and long-term heparin treatment groups. Thus, greater than or equal to 4 days of intravenous heparin therapy after successful streptokinase therapy in AMI is more effective in maintaining short-term infarct vessel patency than a shorter duration of therapy and it may maintain the short-term patency of the infarct vessel in those patients who later spontaneously recanalize.

Diastolic dysfunction during acute cardiac allograft rejection.

Left ventricular diastolic function was evaluated in 41 heart transplant patients during acute rejection by an analysis of echocardiograms and surgically implanted intramyocardial tantalum markers. In 35 patients, isovolumic relaxation time was calculated from M-mode tracings selected from two-dimensional echocardiographic recordings. A total of 84 biopsy findings of no rejection, moderate rejection, and severe acute rejection after treatment were correlated with measurements of isovolumic relaxation time. In six patients, end-diastolic volume, end-systolic volume, stroke volume, ejection fraction, and peak filling rate were obtained from biplanar cineradiographic images of intramyocardial markers. Data from 11 prerejection periods were compared with those of moderate acute rejection. All echocardiograms and marker images were analyzed without previous knowledge of biopsy findings. At times of acute rejection, isovolumic relaxation time decreased from 107 to 65 msec (p less than 0.01) and returned to 98 msec after immunosuppressive therapy. Ejection fraction and end-systolic volume did not change significantly with acute rejection, whereas stroke volume decreased from 76 to 67 ml (p less than 0.05). In contrast to the effects on systolic function, episodes of acute rejection were accompanied by a decrease in end-diastolic volume from 166 to 153 ml (p less than 0.01) and a reduction in peak filling rate from 514 to 460 ml/sec (p less than 0.05). These data suggest that acute cardiac rejection is associated with relative preservation of left ventricular systolic performance but with alterations in diastolic dynamics similar to those seen in "restrictive" cardiomyopathy.

Effects of intravenous verapamil on left ventricular systolic function and diastolic filling dynamics in patients with coronary artery disease: analysis of intramyocardial markers.

Left ventricular (LV) intramyocardial markers (MM) were used to study the effects of intravenous verapamil on LV pump function and diastolic filling dynamics. Verapamil (0.1 mg/kg bolus followed by 0.005 mg/kg/min) was administered to 10 patients with severe coronary artery disease 4 years after coronary bypass grafting and implantation of 7 tantalum markers into the LV. MM were filmed at 100 frames/sec (biplane 30 degrees RAO/60 degrees LAO). The digitized biplane MM coordinates were transformed into 3-dimensional coordinates and maximal projection area was defined. LV volumes were calculated frame-by-frame and ejection fraction and peak filling rate derived. Pressure-volume relations were calculated in early-, mid-, and end-diastole. Verapamil caused a slight rise in end-diastolic pressure (12 to 14 mmHg, p less than 0.001) and end-diastolic volume (142 to 152 ml; p less than 0.005) and a fall in max dP/dt (1732 to 1570 mmHg/s; p less than 0.01) reflecting the drug's negative inotropic action. Verapamil reduced LV systolic pressure (136 to 126 mmHg; p less than 0.01), diastolic aortic pressure (74 to 68 mmHg; p less than 0.001) and peripheral resistance (1496 to 1348 dynes.s.cm-5; p less than 0.025); cardiac index was increased (2.7 to 2.9 l/min/m2; p less than 0.05), as were ejection fraction (47 to 49%; p less than 0.02) and stroke volume (67 to 75 ml; p less than 0.001). Great cardiac vein flow increased as well (88 to 102 ml/min; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute percutaneous transluminal coronary angioplasty complicated by embolism to a coronary artery remote from the site of infarction.

Percutaneous transluminal coronary angioplasty has emerged as a mode of treatment in patients with both chronic and acute coronary syndromes. Among the recognized complications of coronary angioplasty is coronary embolism. This case report describes a case of acute anterior myocardial infarction which was treated with angioplasty of the left anterior descending coronary artery. Postdilation angiography revealed obstruction of the posterior descending artery (in a left dominant system). The use of thrombolytic therapy previous to angioplasty is briefly discussed.

Morphology of occlusive coronary lesions during acute myocardial infarction: an angiographic and clinical analysis.

In an attempt to identify angiographic and clinical predictors of reperfusion, 42 patients who received intracoronary streptokinase during the early phase of myocardial infarction were analyzed. The different morphologies (regular and irregular) of the occlusive lesions did not show a significant relation with the response (reperfusion vs nonreperfusion) to intracoronary streptokinase; neither did the presence of angiographically visualized thrombus in the infarct-related artery favor reperfusion. Among the clinical variables analyzed (previous myocardial infarction, previous angina, diabetes mellitus, hypertension, use of tobacco, and hyperlipidemia), a history of previous angina was significantly related to absence of reperfusion (p = 0.001). Although the presence of thrombus showed a trend toward reperfusion (p = 0.1), overall, our angiographic observations did not contribute to predicting the response to streptokinase. Further studies are needed to identify morphologic criteria favoring reperfusion and select groups of patients most likely to benefit from it.

[Acute effect of the cardioselective beta-1-partial agonist, Corwin, on ventricular function and myocardial oxygen consumption in patients with dilated cardiomyopathy]. / Die akute Wirkung des kardioselektiven beta-1-partiellen Agonisten, Corwin, auf die Ventrikelfunktion und den myokardialen Sauerstoffverbrauch bei Patienten mit dilativer Kardiomyopathie.

The effects on left ventricular function and myocardial metabolism of Corwin (ICI 118,587), a selective beta-1 partial agonist, were evaluated in 12 patients with dilated cardiomyopathy. All patients were in sinus rhythm at the time of cardiac catheterization. Immediately before and 20 minutes after intravenous administration of 0.2 mg/kg Corwin over 2 minutes, high-fidelity left ventricular pressures and thermodilution coronary sinus blood flow were recorded along with ventriculograms in the 30 degrees right anterior oblique projection. In 11 patients, Corwin resulted in no change in heart rate, a fall in left ventricular end-diastolic pressure, a rise in left ventricular systolic pressure and an increase in cardiac index. There was a rise in both peak positive and peak negative dP/dt. End-diastolic and end-systolic volume indices fell, and ejection fraction rose. There was an increase in coronary sinus blood flow and a small rise in myocardial oxygen consumption. In contrast to these results in the group as a whole, in one patient Corwin produced depression of both systolic and diastolic left ventricular function. We conclude that, in many patients with dilated cardiomyopathy, Corwin produces an improvement in systolic and diastolic left ventricular function while at the same time only slightly increasing myocardial oxygen demand. In some patients, however, Corwin may result in a significant worsening of left ventricular performance due to its antagonistic effects.

Collateral flow in patients with acute myocardial infarction.

To assess the change in angiographically visualized collaterals in evolving acute myocardial infarction (AMI), coronary arteriograms from 53 patients obtained 6.2 +/- 0.2 hours after onset of AMI symptoms were compared with follow-up angiograms obtained 14 +/- 1 days later. Collaterals were graded according to intensity score and percent of distal infarct-related artery visualized. Collateral intensity score and the percent of distal infarct vessel visualized by collaterals at baseline were low, and there was a significant increase in both values at follow-up angiography. The group of 20 patients with occluded infarct vessels at follow-up study accounted for these increases. In 33 patients with patent infarct vessels at repeat angiography, collateral intensity score and percent of segment visualized were unchanged. Among the patients with occluded infarct vessels at baseline and subsequent improvement in left ventricular (LV) ejection fraction (EF), baseline collateral score and percent of segment visualized were significantly greater than in patients in whom LVEF did not improve. Thus, in patients with evolving AMI, (1) angiographically visible collaterals are not extensive within the early hours of AMI, (2) the extent of collaterals on follow-up angiography may not be representative of that on the day of AMI, (3) collaterals are considerably more common 2 weeks after AMI, especially in patients with occluded infarct arteries during follow-up, and (4) collaterals present at the time of AMI are associated with improved LVEF at 2 weeks.

Chronic aortic regurgitation: reassessment of the prognostic value of preoperative left ventricular end-systolic dimension and fractional shortening.

The prognostic significance of a preoperative echocardiographic left ventricular end-systolic dimension (ESD) greater than 55 mm and/or fractional shortening (FS) of 25% or less was evaluated retrospectively in 84 patients who had undergone aortic valve replacement for isolated chronic aortic regurgitation due to various causes. Postoperative survival, improvement in symptoms, and echocardiographic evidence of regression of left ventricular dilatation and hypertrophy were compared between patients with a preoperative ESD greater than 55 mm (category 1) and those with an ESD of 55 mm or less (category 2) and between patients with FS of 25% or less (category 3) and those with FS greater than 25% (category 4). Patients in categories 1 and 3 had a higher preoperative left ventricular end-diastolic dimension (EDD) and cross-sectional area than those in categories 2 and 4, respectively, but their preoperative functional impairment (NYHA class) was similar. There were 13 deaths, only two of which (one early, one late) could be attributed to left ventricular dysfunction. In both, FS was 25% or less and in one ESD was greater than 55 mm. There was a weak association without useful positive predictive value between the echocardiographic variables and postoperative death due to all causes. Among 42 patients with a preoperative ESD greater than 55 mm and/or FS of 25% or less, 33 (79%) were alive at a mean follow-up of 29.5 months. Symptoms improved in all categories of survivors, with the postoperative NYHA class being similar between categories 1 and 2 and between categories 3 and 4. Among 48 survivors with high-quality echocardiograms both before and after surgery, EDD fell in all groups but fell to a lesser extent in category 3 than in category 4. Postoperative cross-sectional area fell to the same level in all categories. Follow-up intervals were similar in all categories. We conclude that in patients undergoing aortic valve replacement for chronic aortic regurgitation, a preoperative ESD greater than 55 mm or an FS of 25% or less does not reliably predict early or late death, does not correlate with lack of improvement in symptoms, and does not preclude postoperative regression of left ventricular dilatation and hypertrophy. Thus these echocardiographic criteria alone cannot be used for the timing of surgical intervention in these patients.

Return of left ventricular function after reperfusion in patients with myocardial infarction: importance of subtotal stenoses or intact collaterals.

To determine whether subsequent improvement in left ventricular ejection fraction can be predicted from preintervention coronary arteriograms, we divided 63 patients with acute myocardial infarction into two groups based on findings at emergency coronary arteriography at a mean of 7 hr after onset of symptoms: (1) a "no-flow" group with an occluded infarct-related artery and no easily visible collaterals (n = 36) and (2) a "limited-flow" group with either subtotal stenosis or total occlusion of the infarct-related vessel with intact collaterals (n = 27). Of the 63 patients, 61 underwent emergency procedures to establish reperfusion. At follow-up angiography (contrast or radionuclide) performed 12 +/- 7 days after infarction, global ejection fraction had increased significantly in patients with limited flow to the infarct zone and "successful" early reperfusion intervention due primarily to a significant increase in the regional ejection fraction in the infarct zone. Global ejection fraction fell significantly between baseline and follow-up in patients with no flow to the infarct zone and "unsuccessful" early reperfusion intervention due primarily to a fall in the regional ejection fraction of the noninfarct zone. Global and regional ejection fractions did not change significantly in patients with no flow to the infarct zone and successful early reperfusion or in patients with limited flow to the infarct zone and unsuccessful early reperfusion intervention. The elapsed time before reperfusion did not relate significantly to the change in either regional or global ejection fraction. However, the magnitude of improvement in both global and regional ejection fraction at follow-up was greater among patients with anterior infarcts than among those with inferior infarcts, possibly because baseline ejection fraction was lower in patients with anterior infarcts. These data indicate that among patients with acute myocardial infarction undergoing emergency coronary arteriography at a mean of 7 hr after onset of symptoms, improvement in global ejection fraction is unlikely to occur even after a successful early reperfusion intervention in the absence of preserved flow to the infarct area. However, among patients with subtotally occluded infarct-related arteries or significant collateral blood flow to the infarct zone, subsequent improvement in global and regional ejection fraction in the zone of myocardial infarction frequently occurs. Improvement in both global and regional ejection fraction may be more readily demonstrated in patients initially having more severe depression of these parameters.

[Hemodynamics in ischemia: diastolic phase]. / Hämodynamik unter Ischämie: Diastolische Phase.

The diastolic portion of the cardiac cycle can be divided into sequential phases: isovolumic ventricular relaxation; rapid ventricular filling; slow, or passive, ventricular filling; and atrial contraction. Contraction and relaxation are to some extent interrelated; however, relaxation is not simply a passive reversal of events during systole. Rather, relaxation is an energy-consuming process which involves dissociation of calcium from the actin-myosin-complex and reuptake of calcium by the sarcoplasmic reticulum. Left ventricular diastolic function is determined by the interrelationship of several/factors, including some intrinsic to the left ventricular chamber (completeness of left ventricular relaxation, time course of left ventricular contraction, and elastic and viscous properties of the myocardium) and others extrinsic to the left ventricle (pericardial and pleural pressure, right ventricular contraction, and coronary perfusion pressure). Acute ischemia alters diastolic left ventricular function by: slowing isovolumic relaxation, delaying left ventricular filling and altering passive elastic properties of the myocardium. Slowing of isovolumic relaxation is measured as a fall in the maximal rate of left ventricular pressure decline (peak negative dP/dt) and as an increase in the time constant (T) of left ventricular pressure fall. Delayed left ventricular filling is manifested regionally as a reduced rate of septal and posterior wall thinning (by echocardiography) and globally as a reduced rate of chamber filling (by gated radionuclide angiography).(ABSTRACT TRUNCATED AT 250 WORDS)

Intracoronary nifedipine in human beings: magnitude and time course of changes in left ventricular contraction/relaxation and coronary sinus blood flow.

Eight patients, all men, having at least 75% stenosis of the proximal, middle or both segments of the left anterior descending coronary artery, underwent intracoronary drug studies at the time of cardiac catheterization after saphenous vein bypass grafting. Nifedipine, 0.1 mg dissolved in saline solution, was infused into a left anterior descending graft that was the primary blood supply to each patient's anterior left ventricular wall and septum. High fidelity left ventricular pressure and its first derivative, dP/dt, and aortic pressure were sampled synchronously with coronary sinus blood flow by the thermodilution technique. The time constant of isovolumic pressure decay (T) was derived. In five patients, percent systolic shortening and mean shortening velocity were determined from myocardial markers implanted into the midwall of the myocardium at the time of cardiac surgery. In response to nifedipine, left ventricular systolic pressure decreased and end-diastolic pressure increased up to 60 seconds. Both positive and negative dP/dt also decreased up to 60 seconds, whereas coronary sinus blood flow increased up to 5 minutes. T was increased at 1 minute but returned to baseline by 3 minutes. Percent systolic shortening and mean shortening velocity were decreased at 1 minute but returned to control level by 3 minutes. Thus, although both left ventricular systolic and diastolic function were depressed by intracoronary administration of nifedipine, coronary sinus blood flow was augmented and remained increased long after changes in left ventricular contraction and relaxation had subsided. These temporal differences are consistent with animal studies showing a differential depressant effect of nifedipine on calcium uptake in smooth muscle and cardiac muscle.

Prospective randomized trial of intravenous and intracoronary streptokinase in acute myocardial infarction.

To evaluate the relative thrombolytic efficacy and complications of intracoronary vs high-dose, short-term intravenous streptokinase infusion in patients with acute myocardial infarction, we performed baseline coronary arteriography and then randomly allocated 51 patients with acute myocardial infarction to receive either intracoronary (n = 25) or intravenous (n = 26) streptokinase. Patients getting the drug by the intracoronary route received 240,000 IU of streptokinase into the infarct-related artery over 1 hr, whereas those getting the drug by the intravenous route received either 500,000 IU of streptokinase over 15 min (n = 10) or 1 million IU of streptokinase over 45 min (n = 16). Angiographically observed thrombolysis occurred in 76% (19/25) of the patients receiving intracoronary streptokinase, in 10% (1/10) of the patients receiving 500,000 IU of streptokinase intravenously, and in 44% (7/16) of the patients receiving 1 million IU of streptokinase intravenously. Among patients in whom thrombolysis was observed, mean elapsed time from onset of streptokinase infusion until lysis was 31 +/- 18 min in patients receiving intracoronary streptokinase and 38 +/- 20 min in those receiving intravenous streptokinase (p = NS). Among patients in whom intravenous streptokinase "failed," intracoronary streptokinase in combination with intracoronary guidewire manipulation recanalized only 7% (1/15). Fibrinogen levels within 6 hr after streptokinase were significantly lower in the patients receiving intravenous streptokinase (39 +/- 17 mg/dl) than the levels in those receiving intracoronary streptokinase (88 +/- 70 mg/dl) (p less than .05) but were similar 24 hr after streptokinase in the two groups. Bleeding requiring transfusion occurred in one patient in each group. Thus, in this prospective randomized trial of intracoronary vs intravenous streptokinase, hemorrhagic complications were few, although both regimens produced a systemic lytic state. Although the thrombolytic efficacy of intracoronary streptokinase was superior to that of high-dose, short-term intravenous streptokinase, the higher-dose intravenous regimen (1 million IU over 45 min) achieved thrombolysis in a significant minority (44%) of patients and might be useful therapy for patients not having access to emergency catheterization.

Effects of nitroglycerin on left ventricular diastolic properties in man.

The effects of nitroglycerin (NTG) on left ventricular (LV) isovolumic relaxation and diastolic function were studied in 12 patients with coronary artery disease: in 6 patients after 0.8 mg sublingual (sI) NTG and in 6 patients after 0.15 mg intracoronary (ic) NTG. From high-fidelity LV pressure peak positive and negative dP/dt, LV systolic (LVSP) and end-diastolic pressure (LVEDP) were measured. The time constant T of isovolumic pressure decay was derived from P = a X exp(-t/T) + c. From simultaneous diastolic pressures and volumes, pressure-volume curves were obtained throughout diastole. In an additional 14 patients, the effects of 0.15 mg ic NTG on coronary sinus blood flow (CSBF) and end-diastolic (ED) and end-systolic septal thickness (ESST) were evaluated. SI NTG produced an increase in heart rate and a decrease in LVSP, LVEDP and negative dP/dt. These effects were associated with a decrease in T and a downward shift of the pressure-volume relation. In contrast, ic NTG caused no change in heart rate, LVSP and LVEDP. The LV pressure-volume relation was not altered although T decreased. Ic NTG produced an early rise in CSBF and a sustained increase in EDST and ESST. Data indicate that sI NTG increases the speed of isovolumic relaxation and improves diastolic function, but these actions are not reflected by negative dP/dt due to its dependence on multiple hemodynamic factors. Ic NTG accelerates isovolumic relaxation, but has no measurable effects on later diastolic function. The increase in positive dP/dt may be explained by an engorgement of the coronary vasculature resulting in stretching of the myocardial fibers.

The importance of angled right anterior oblique views in improving visualization of the coronary arteries. Part I: Caudocranial view.

Three hundred patients were examined to determine the value of the caudocranial right anterior oblique view (RAO) in revealing or improving visualization of lesions in the proximal and mid-left anterior descending artery (LAD), the origins of the septal and diagonal arteries, and the distal branches of the right coronary artery (RCA). The proximal and mid-LAD were shown to greater advantage in 80% of cases, the diagonal arteries in nearly 75%, the septal vessels in more than 90%, and the posterior descending and posterolateral branches of the distal RCA in more than 80%; in addition, the cranial RAO view revealed previously unsuspected lesions in 7% of the proximal and mid-LAD arteries and 26% of the septal vessels. In addition to superior visualization, this view gives satisfactory exposure even in extremely large patients and may also be helpful in coronary angioplasty.

The importance of angled right anterior oblique views in improving visualization of the coronary arteries. Part II: Craniocaudal view.

The craniocaudal right anterior oblique view (RAO) of the left coronary artery was employed for 100 angiograms. Visualization of the proximal and left distal circumflex, first and second marginal, and proximal left anterior descending artery (LAD) and its branches was compared with that on the non-angled RAO projection. Diagnostic accuracy was increased with the caudal RAO view in 88% of proximal circumflex segments, 69% of distal circumflex segments, 52% of first marginal segments, 33% of second marginal segments, and 33% of proximal LAD systems. Of 68 lesions identified, 15 (22%) were seen only on the caudal RAO view. The authors feel that this projection is a valuable and necessary addition to routine views of the left coronary artery, and that optimum evaluation is achieved by routine use of a combination of caudal, non-angled, and cranial RAO views.