Intracoronary Injection Of Nitroglycerin Research Articles

Severe coronary artery spasm during left atrial appendage closure plus catheter ablation for atrial fibrillation: case presentation

BackgroundLeft atrial appendage closure (LAAC) combined with radiofrequency catheter ablation (RFCA) as a hybrid procedure is commonly performed to treat atrial fibrillation (AF). Although this treatment carries a low risk of coronary artery spasm (CAS), and has never been observed in LAAC procedure, caution still needed to be taken. We presented a case of CAS that occurred in an AF patient during the hybrid procedure.Case presentationThe patient was a 65-year-old man with paroxysmal AF who developed CAS during RFCA and LAAC. In this case, LAAC was performed ahead of RFCA. After atrial septal puncture, the occluder was advanced into left atrium through delivery sheath, and successfully deployed in the LAA. After verifying the assessment of “PASS” criteria, we decided to release the device. However, before releasing the occluder in LAAC, the patient’s blood pressure (BP) fell to 70/45 mmHg with heart rate (HR) drop and ST-segment elevation in II, III, and aVF and reciprocal ST-segment depression in I and aVL. Isotonic sodium chloride load was administered. After 3 min, the BP and HR raised, and ST-segment returned to normal. The occluder was successfully released after the stable condition of the patient. Then, RFCA was sequentially performed. When isolating the right pulmonary veins, the patient’s BP and HR fell again with ST-segment elevation in inferior leads. Spontaneous ventricular tachycardia and fibrillation developed rapidly and defibrillation was performed immediately with success. Coronary angiography revealed the obstruction of the right coronary artery which disappeared completely after intracoronary nitroglycerin injection (1 mg). Under systemic diltiazem infusion, the RFCA procedure was accomplished. After the procedure, the patient recovered without any neurologic deficit, and CAS has never recurred with isosorbide mononitrate treatment during follow-up.ConclusionsCAS is a rare complication associated with AF hybrid procedure. Attention should be paid to this rare but potentially life-threatening complication.

In-Hospital Cardiac Arrest after Emotional Stress in a Patient Hospitalized with Gastrointestinal Symptoms and Chronic Anxiety Disorder

Background: We report an acute emotional stress–induced in-hospital cardiac arrest in a patient admitted with gastrointestinal symptoms after experiencing chronic anxiety disorder. Case Presentation: The patient was admitted to the Second Xiangya Hospital, Central South University, with gastrointestinal symptoms and chronic anxiety disorder, and experienced cardiac arrest during hospitalization after acute emotional stress. Malignant ventricular tachycardia and cardiogenic shock were evidenced in this patient after the acute emotional stress. Severe and extensive coronary spasm was confirmed by emergency coronary angiography, and coronary spasm was relieved by intracoronary injection of nitroglycerin. The patient recovered from myocardial infarction with nonobstructive coronary arteries. However, the patient developed acute kidney dysfunction and severe pulmonary infection and eventually died of respiratory circulatory failure on the ninth day after the successful rescue. Conclusions: Acute emotional stress on top of chronic anxiety disorder in patients hospitalized for noncardiovascular reasons might lead to the development of life-threatening cardiovascular diseases, including coronary artery spasm and myocardial infarction with nonobstructive coronary arteries. Psychological management is of importance to improve the outcome of these patients.

Intracoronary nitroglycerin injection through a homemade side-hole ballon for coronary slow/no-reflow phenomenon prevention

Abstract Objective The evaluate nitroglycerin-injection during the homemade side-hole ballon into the proximal segment of the target lesion by TIMI blood flow and the corrected TIMI frame count (CTFC) during primary PCI for patients with ST-segment elevation myocardial infarction (STEMI). Methods All patients were diagnosed with STEMI. A dual antiplatelet therapy was given; patients were able to receive pPCI. The basic TIMI blood flow and CTFC were recorded after angiography and randomized according to the random number table by group A (n=61, early nitroglycerin injection via side-hole ballon) andgroup B (n=59, Traditional protocol PCI). Side-hole ballon was made by the ballon that passed the target lesion and puncture it with holes with needle. The TIMI blood flow and CTFC status immediately after the pPCI and the related events during the hospitalization and 6 months discharged. Results There were no significant differences between the baseline and laboratory parameters of the two groups (P>0.05). Also no differences in TIMI blood flow and CTFC frame before the target vessel was opened (P>0.05), Further no difference in number of implanted stents, stent length and diameter. The immediate effect after pPCI showed, the early nitroglycerin injection via side-hole ballon have effect on the TIMI blood flow (P=0.027), the CTFC (P=0.007) and the proportion of slow/no-reflow (6.56% vs. 22.03%, P=0.015). There was no difference in the incidence of MACE between two groups during hospitalization and 30 days follow-up. The incidence of MACE at 6 months follow-up was significantly lower in group A (1.63% vs. 10.17%, P=0.046). Conclusion In pPCI process, the early upstream nitroglycerin injection via homemade side-hole ballon can significantly reduce the incidence of slow/no-reflow after pPCI while the guidewire/balloon passes through the lesion. After pretreatment by this manner, the patient's 6-month MACE rate can be significantly improved. Figure 1 Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): The basic research project of Anhui Medical University

Coronary vasospasm caused by local infiltration of epinephrine after spinal anesthesia.

Coronary vasospasm caused by local infiltration of epinephrine after spinal anesthesia.

Instabile Angina pectoris: Zusammenspiel von epikardialer Stenose und Prinzmetal-Spasmus

A 61-year-old man presented with recurrent angina pectoris at rest for 3 days. The medical history revealed hypertension and an elevated cholesterol level as cardiovascular risk factors. The physical examination revealed no pathological findings. ECG at admission showed no signs of ischemia, while high-sensitive Troponin T was slightly elevated. Echocardiography showed diastolic dysfunction and biatrial dilatation. During another episode of angina at rest, ECG showed T-wave inversion in lead aVL. Therefore, coronary angiography was performed. At the beginning of the examination the patient complained of angina at rest and ECG showed ST-elevation in the inferior leads. Coronary angiography revealed a subtotal stenosis in the middle part of the RCA. After intracoronary nitroglycerin injection there was a high-grade stenosis in this region. An intracoronary acetycholin provocation test was performed which reproduced a focal spasm in the area of the RCA stenosis with simultaneous changes in the ECG and reproduction of the patient's unusual angina. After implantation of a bare metal stent a subsequent ACH-test did not elicit any further coronary spasm. Four weeks after the procedure the patient had no further complaints under medical treatment. This case illustrates a patient with a focal Prinzmetal-type spasm with ST-elevation on top of a high-grade stenosis of the right coronary artery as an explanation for the unstable angina. Coronary spasm of the Prinzmetal-type can occur in vessels with epicardial stenosis as well as in vessels without stenosis. In some cases focal coronary spasm can be prevented by the implantation of a stent.

Transient Impairment of Vasomotion Function After Successful Chronic Total Occlusion Recanalization

The aim of our study was to assess coronary vasomotion after successful revascularization of chronic total occlusion (CTO). It is largely unknown whether the recovery of anterograde flow after CTO recanalization with drug-eluting stent implantation affects vascular function in distal coronary segments. One hundred consecutive CTOs successfully treated with drug-eluting stents underwent coronary diameter measurement after intracoronary nitroglycerin injection 5, 20, and 35 mm distal to the stented coronary segment using 3-dimensional quantitative coronary angiography. In a subgroup of 14 patients, coronary vasomotion was tested in distal segments: incremental atrial pacing for endothelium-dependent cases; and intracoronary nitroglycerin injection for endothelium-independent cases. In another subgroup of 13 patients, distal vessels were assessed by intracoronary ultrasounds. Vessel diameters significantly increased at follow-up as compared to baseline values (2.0 ± 0.52 mm vs. 2.25 ± 0.50 mm, 1.76 ± 0.49 mm vs. 2.05 ± 0.58 mm, 1.54 ± 0.53 mm vs. 2.04 ± 0.58 mm, at each segment analyzed; p < 0.001). At baseline, distal segments failed to respond to both endothelium-dependent and -independent stimuli. At follow-up, atrial pacing induced vasoconstriction, whereas nitroglycerine administration resulted in significant vasodilation (p < 0.05). Intracoronary ultrasounds failed to show changes of the cross-sectional area of distal segments at follow-up angiography. Recanalization of CTO is followed by a hibernation of vascular wall at distal coronary segments that fail to respond to endothelium-dependent and -independent stimuli. Distal vessel diameter increases over time in the absence of positive remodeling and in spite of persistent endothelial dysfunction. This severe impairment of vasomotor tone after CTO reopening suggests that intracoronary ultrasound assessment is of paramount importance for the selection of stent size.

Ischemia-Induced Prominent J Waves in a Patient with Brugada Syndrome

A 75-year-old man was admitted to our hospital in January 2010 for evaluation of syncope and abnormal ECG. ECG showed type 1 ST elevation in lead V(1) and he was diagnosed as Brugada syndrome. During cardiac catheterization, baseline coronary angiography was normal, but intracoronary ergonovine maleate induced spasms of the right and left coronary arteries concomitant with chest pain and ST elevation on ECG. J waves were accentuated or newly developed. Soon after an intracoronary injection of nitroglycerin, chest pain was relieved and ischemia-induced J wave disappeared and the ST segment returned to the same morphology as baseline. Extrastimuli induced ventricular fibrillation. He received an implantable cardioverter-defibrillator. He was also treated with Ca antagonist and isosorbide dinitrate and has had an uneventful course for 5 months.

Optical Coherence Tomography Findings in a Case of Acute Coronary Syndrome Caused by Coronary Vasospasm

Culprit lesions of acute coronary syndrome (ACS) were observed by intravascular optical coherence tomography (OCT). OCT images revealed diffuse intimal thickening, reduced lumen area with vascular contraction, and thrombus formation. No OCT images of atherosclerotic plaque disruption were found. Vascular contraction disappeared and the lumen was dilated after intracoronary injection of nitroglycerin. The main mechanism of ACS in this case was therefore considered to be coronary vasospasm. OCT may be useful for evaluating the mechanism of ACS.

Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease.

Endothelial vasodilator dysfunction is a characteristic feature of patients at risk for coronary atherosclerosis. Therefore, we prospectively investigated whether coronary endothelial dysfunction predicts disease progression and cardiovascular event rates. Coronary vasoreactivity was assessed in 147 patients using the endothelium-dependent dilator acetylcholine, sympathetic activation by cold pressor testing, dilator responses to increased blood flow, and dilation in response to nitroglycerin. Cardiovascular events (cardiovascular death, unstable angina, myocardial infarction, percutaneous transluminal coronary angioplasty, coronary bypass grafting, ischemic stroke, or peripheral artery revascularization) served as outcome variables over a median follow-up period of 7.7 years. Patients suffering from cardiovascular events during follow-up (n=16) had significantly increased vasoconstrictor responses to acetylcholine infusion (P=0. 009) and cold pressor testing (P=0.002), as well as significantly blunted vasodilator responses to increased blood flow (P<0.001) and the intracoronary injection of nitroglycerin (P=0.001). Impaired endothelial and endothelium-independent coronary vasoreactivity were associated with a significantly higher incidence of cardiovascular events by Kaplan-Meier analysis. By multivariate analysis, all tests of coronary vasoreactivity were significant, independent predictors of a poor prognosis, even after adjustment for traditional cardiovascular risk factors or the presence of atherosclerosis itself. Coronary endothelial vasodilator dysfunction predicts long-term atherosclerotic disease progression and cardiovascular event rates. Thus, the assessment of coronary endothelial vasoreactivity can provide pivotal information as both a diagnostic and prognostic tool in patients at risk for coronary heart disease.

Inappropriate microvascular constriction produced transient ST-segment elevation in patients with syndrome X

Objectives. The aim of this project was to study the responsible site(s) and underlying cardiac disease(s) of patients with transient ST-segment elevation and normal coronary angiograms.Background. Transient ST-segment elevation has been demonstrated in patients with variant angina or unstable angina. In those patients, epicardial coronary arteries, not microvessels, are always the responsible site for the transient ST-segment elevation.Methods. This study consisted of three cases with a transient ST-segment elevation and normal coronary angiograms. Treadmill testings were performed before coronary angiography in all cases. Coronary angiography was undertaken during the control state and during ST-segment elevation and, when possible, a Doppler guide wire was positioned in the left anterior descending artery (LAD). Coronary responses to vasodilators were observed. Finally, cardiac biopsy was performed and pathologic observation was conducted.Results. All three cases had significant ST-segment depression during treadmill testing in II, III, aVF and V4–6leads; however, no angiographic coronary stenosis was demonstrated and vasospasm was not provoked. A transient ST-segment elevation associated with chest pain was observed in V1–5leads, but normal coronary angiograms during ST-segment elevation were observed in every case. Coronary blood flow (CBF) velocity profile remained normal during ST-segment elevation. In one case, vasodilator responses to the LAD during ST-segment elevation were also measured. A 0.5 mg intracoronary injection of nitroglycerin increased CBF velocity (220%), but ST-segment elevation was not normalized and chest pain persisted. A 10 mg intracoronary injection of papaverine (PVN) further increased CBF velocity up to 340%, and this normalized ST-segment elevation and relieved chest pain quickly. Either endothelium-dependent coronary flow reserve (CFR) measured with a 100 μg intracoronary infusion of acetylcholine, or flow-dependent CFR by a 10 mg intracoronary injection of PVN was reduced in one of two cases measured. Pathologic findings supported syndrome X as the underlying cardiac disease in all cases.Conclusions. These findings suggested a new clinical implication involving transient ST-segment elevation mimicking variant angina and normal coronary angiograms in patients with syndrome X. The major responsible site for this phenomenon was suggested to be coronary arterioles of less than 200 μm in diameter.

Effects of enalapril during continuous nitrate therapy: Analysis of diameter of coronary arteries and platelet cyclic guanosine monophosphate

To investigate the effects of enalapril, an angiotensin-converting enzyme inhibitor, on nitrate tolerance during continuous nitrate therapy, coronary artery diameters and platelet cyclic guanosine monophosphate (cGMP) levels were measured before and 2 minutes after intracoronary injection of nitroglycerin 200 μg in 60 patients with coronary artery disease and were compared among 20 patients treated with nitrates (nitrate group), 20 patients treated with both nitrates and enalapril (enalapril group), and 20 untreated patients (control group). The percent increase in platelet cGMP and coronary dilatation in the nitrate group was significantly less than in the control group, but the percent increase in the enalapril group was significantly greater than that in the nitrate group. These results indicate that enalapril may be helpful as concomitant therapy to maintain the effect of nitrates during continuous nitrate therapy. (Am Heart J 1997;134:614-21.)

Preferential dilation of recipient coronary arteries of the collateral circulation by intracoronary administration of nitroglycerin

Objectives. The purpose of this study was to test the hypothesis that the sensitivity to nitroglycerin of collateral vessels and recipient arteries is greater than that of donor arteries of the collateral circulation.Background. The collateral circulation responds vigorously to nitroglycerin. However, the mechanisms of the efficacy of nitroglycerin for improving collateral circulation are not fully elucidated.Methods. The diameter of donor and recipient arteries of the collateral circulation was measured with a computer-assisted analysis system in eight patients with well developed collateral vessels. Coronary angiography was repeated before and after the intracoronary injection of 50 μg of nitroglycerin.Results. After nitroglycerin, the mean diameter ± SD of donor arteries increased to 1.61 ± 0.53 from 1.29 ± 0.39 mm (p < 0.01), whereas the diameter of recipient arteries increased to 1.59 ± 0.50 from 1.10 ± 0.49 mm (p < 0.01). The change in the diameter of recipient arteries was significantly greater than that of donor arteries (52.3 ± 24.6% vs. 24.7 ± 11.5%, p < 0.05). These changes induced by the intracoronary injection of nitroglycerin were accompanied by a decrease in pacing-induced ST segment depression (0.16 ± 0.06 to 0.06 ± 0.04 mV, p < 0.01), suggesting increased flow reserve through collateral channels.Conclusions. These findings indicate that the sensitivity to nitroglycerin of recipient arteries of the collateral circulation is significantly greater than that of donor arteries. This observation may explain the strong response of the collateral circulation to nitroglycerin in patients with functionally significant collateral channels.

Effects of intracoronary administration of nitroglycerin on contralateral intracoronary acetylcholine test results

This study examined the question of whether intracoronary administration of nitroglycerin modifies contralateral intracoronary acetylcholine test results. Acetylcholine was injected separately into both left and right coronary arteries in 63 patients with coronary spastic angina. Acetylcholine (20 and 50 micrograms) was injected first into the coronary artery responsible for the documented regional ischemia during spontaneous or induced attacks, and then into the other coronary artery. Coronary spasm was defined as severe transient coronary artery vasoconstriction with chest pain and/or electrocardiographic ischemic ST-segment deviation. Spasm was induced in either coronary artery in 60 patients (95%) and in both coronary arteries in 23 patients (37%). The frequency of induced spasm was 67% (42 of 63) in the coronary artery first challenged by acetylcholine. The coronary artery spasm subsided with the intracoronary injection of nitroglycerin (250-750 micrograms) in 19 patients. In the second challenge of intracoronary acetylcholine injection into the contralateral coronary artery, coronary spasm was induced in 29 (66%) of 44 patients. This was done without intracoronary administration of nitroglycerin in the first challenge and in 12 (63%) of 19 patients who had been given intracoronary nitroglycerin. The sensitivity for spasm induced by intracoronary acetylcholine appeared to be unaffected by nitroglycerin. Coronary spasm with ST-segment elevation by intracoronary acetylcholine in the second challenge was significantly less frequent in the patients receiving intracoronary acetylcholine in the second challenge was significantly less frequent in the patients receiving intracoronary nitroglycerin (first: 89%, second: 26%, p < 0.05) as well as in those not receiving intracoronary nitroglycerin for the spasm in the first challenge (first: 52%, second: 13%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Intracoronary thrombus formation causes focal vasoconstriction of epicardial arteries in patients with coronary artery disease.

Experimental studies have demonstrated that intracoronary platelet aggregation and thrombus formation may induce marked vasoconstriction of epicardial arteries with endothelial injury. To examine the effects of intracoronary thrombus formation on coronary vasomotor tone of human epicardial arteries in vivo, we studied 15 patients who developed intracoronary thrombi adherent to the guide wire during balloon dilatation. Epicardial artery luminal area was evaluated by quantitative coronary angiography proximal and distal to the site of intracoronary thrombus formation and in a reference vessel before and after thrombus formation as well as after intracoronary injection of 0.2-0.3 mg nitroglycerin. All artery segments distal to the site of thrombus formation showed vasoconstriction with a luminal area reduction of -27.4 +/- 17.1% (p less than 0.001), whereas proximal vessel segments and reference vessels not manipulated during percutaneous transluminal coronary angioplasty did not demonstrate any significant luminal area changes during thrombus formation. Angiographic measurements after advancing the guide wire with the adherent thrombus (performed in six of the 15 patients) revealed in all patients that vasoconstriction did develop at a new site distal to the thrombus persistence of the initial vasoconstriction now residing proximal to the thrombus. Thus, there was a sequential association between thrombus formation and subsequent distal vasoconstriction. Intracoronary injection of nitroglycerin abolished the thrombus-induced vasoconstriction. No significant luminal area changes were observed in 20 patients without angiographic evidence of intracoronary thrombus formation. Intracoronary thrombus formation during percutaneous transluminal coronary angioplasty causes focal vasoconstriction of epicardial arteries in patients with coronary artery disease. Although caution must be advised in the extrapolation of this phenomenon, which was observed in a manipulated artery during coronary angioplasty, the vasoconstrictor response to intracoronary thrombus formation in vivo may play an important role in the dynamic mechanisms of acute coronary heart disease syndromes.

Comparative effects of intracoronary vasodilators on restoring coronary perfusion during flow-reducing coronary stenosis in the dog

The effects of intracoronary injection of nitroglycerin, adenosine, nifedipine and prostacyclin on restoring coronary perfusion during flow-reducing partial coronary obstruction in anesthetized dogs were studied. Coronary obstruction was obtained by inflation of an intraluminal balloon to decrease coronary blood flow and rate of rise in left ventricular pressure (dP/dt) by approximately 30 to 40 and 10%, respectively. Nitroglycerin (0.01 to 10 micrograms/kg per min) increased coronary blood flow and distal coronary pressure and decreased stenosis resistance associated with improved left ventricular dP/dt depending on its dose. In contrast, adenosine (0.3 to 1.0 micrograms/kg per min) decreased coronary blood flow and distal coronary pressure and intensified stenosis resistance associated with depression of left ventricular dP/dt. Nifedipine and prostacyclin caused divergent effects on the coronary circulation related to each dose. Nifedipine (0.01 and 0.1 micrograms/kg per min) and prostacyclin (0.01 micrograms/kg per min) increased coronary blood flow and distal coronary pressure and reduced stenosis resistance. Nifedipine (1.0 micrograms/kg per min) and prostacyclin (0.3 micrograms/kg per min) did not increase coronary blood flow, but reduced distal coronary pressure and intensified stenosis resistance. Thus, the vasodilators produced different effects on restoration of coronary perfusion during pliable severe coronary stenosis. Nitroglycerin and lower doses of nifedipine and prostacyclin improved coronary perfusion due to selective or preferential dilation of large coronary arteries. Adenosine and higher doses of nifedipine and prostacyclin had deleterious effects on the coronary circulation due to potent arteriolar vasodilation.

Exercise-induced plaque rupture producing myocardial infarction

A 37-year-old man with unstable angina was subjected to coronary angiography. The right coronary artery showed a minor proximal stenosis, but there were no obstructive lesions in the left coronary artery. He developed a small inferior infarction. He was asymptomatic until re-admission 1 month later, 1 hour after a normal exercise test, with anterior myocardial infarction. Acute coronary angiography showed sub-total occlusion of the left anterior descending artery. The occlusion was partially relieved after intracoronary injection of nitroglycerin. Intracoronary infusion of streptokinase had no further effect. Balloon angioplasty was then successfully performed. It is suggested that stress-induced plaque rupture with intimal hemorrhage and secondary spasm resulted in sub-total occlusion of the left anterior descending artery producing the second myocardial infarction.

Late phase of nitroglycerin-induced coronary vasodilatation blunted by inhibition of prostaglandin synthesis.

In chloralose-anesthetized dogs with the left circumflex coronary artery perfused at constant flow, the effects of increasing doses of indomethacin or naproxen on the coronary and systemic hemodynamic responses to a 5 microgram intracoronary injection of nitroglycerin (NTG) were evaluated. The integrated areas of NTG-induced coronary vasodilatation were reduced after administration of indomethacin or naproxen. The extent of this reduction was increased progressively by augmenting the dose of indomethacin and naproxen up to 1.5 and 7 mg/kg, respectively. We also assessed the extent of cyclooxygenase inhibition induced by indomethacin or naproxen through the radioimmunoassay of thromboxane B2, which reflects thrombin-induced activation of platelet thromboxane A2 production during whole blood clotting. The level of inhibition progressively increased and complete inhibition was attained with 1.5 mg/kg indomethacin and 7 mg/kg naproxen. Further increase in dosage failed to induce further reduction of integrated areas of coronary vasodilatation, and a correlation was found between the extent of the reduction of the integrated areas of coronary vasodilatation and the dose of indomethacin (r = .828, n = 35, p less than .001) or naproxen (r = .729, n = 35, p less than .001). Finally, the NTG-induced maximum fall in coronary perfusion pressure remained unmodified after inhibition of prostaglandin synthesis, but there was a faster return of the perfusion pressure to the basal value.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Arterial Spasm and Vasomotion (Part 2): Current Concepts Regarding their Role in Ischemic Heart Disease

Acxrst MYOCARDIAL INFARCTION Formany years, coronary th ombosis wacon sidered the sole and immediate cause of myo cardial infarction. This conclusion was understand ably reached because of the high prevalence of coronary thrombi in fatal acute infarction when death occurred more than six hours after the onset of symptoms. It was assumed that the thrombus was present at the moment of infarction and mi tiated the event. In fact, however, the pathologist is hindered in his attempts to understand the initia lion of infarction because myocardial necrosis can not be detected by conventional hematoxylin-eosin stain and light microscopy until six or more hours have elapsed. Electron microscopy and dehydro genase stains allow earlier detection of infarction, but nevertheless, it is not possible to confidently diagnose acute infarction during the critical early hours. Consequenfly, the presence and prevalence of coronary thrombosis at the time infarction begins is unknown. When the onset of chest pain, rather than the presence of necrosis, is used to signal the time of infarction, a thrombus is rarely found when death occurs within an hour or two.36'37 In two patients who died suddenly after the occurrence of chest pain and in one instance ST-segment elevation as well, a ruptured plaque with platelet aggregates adhering to subintimal collagen was present, but no occlusive thrombus had formed by the time of death.37 This suggests that some factor other than thrombosis caused the acute plaque changes and, pan passu, myocardial infarction. Recent clinical observations have established that a coronary thrombus is often present as early as two to six hours after the onset of an infarction and that the thrombus can be lysed by intracoronary streptokinase.@'39 However, this does not preclude the possibility that spasm and or plaque rupture did not occur earlier and lead to occlusion of the vessel and, subsequently, thrombosis. Failure to detect spasm in many of these patients may be due to a number of reasons : 1 ) spasm has not been systematically sought by the intracoronary injection of nitroglycerin before streptokinase administra tion; 2 ) spasm may be refractory even to intra coronary nitroglycerin; 3 ) intracoronary nitroglyc erin is given as a bolus injection over 30 seconds while intracoronary streptokinase is given as a con tinuous infusion over 30 to 90 minutes; 4) intra coronary nitroglycerin is injected into the coronary ostium while intracoronary streptokinase is often injected through a small catheter in close prox imity to the thrombus or the thrombus is pene trated with a guidewire to allow more exposure of the thrombus to the drug. These studies help to fill the void created by the dearth of pathologic information regarding the presence of coronary thrombi during the first few hours of infarction, but they do not help elucidate the initiation of the in farction process.

Excitation of afferent cardiac sympathetic nerves is modulated by nitroglycerin.

AbstractWe examined the effect of nitroglycerin on stimulation of sympathetic nerve fibers arising from receptor sites in the left ventricular wall during acute coronary artery occlusion. Sympathetic afferent nerve activity was recorded in single and multifiber nerve preparations dissected from slips of T3 white rami communicantes. Acute left anterior descending or left circumflex coronary artery occlusion produced an increase in segmental myocardial length and excitation of afferent cardiac sympathetic nerve fibers in the region of the myocardium supplied by the occluded artery. Intravenous administration of nitroglycerin in doses up to 100 μg/kg and sodium nitroprusside (50 μg/min) reduced systolic bulge during coronary occlusions and suppressed excitation of these myelinated and unmyelinated afferent fibers. Local intracoronary injection of nitroglycerin (100 μg) produced neither a change in systemic blood pressure nor a change in excitation of the afferent nerve fibers during coronary occlusion. Syste...

Treatment of prinzmetal's variant angina: Role of medical treatment with nifedipine and surgical coronary revascularization combined with plexectomy

This study describes three forms of treatment of Prinzmetal's variant angina. Coronary spasm, frequently found at coronary arteriography in patients with Prinzmetal's variant angina, can be treated with intravenous or intracoronary injection of nitroglycerin as well as of nifedipine. Nifedipine (0.2 mg) was injected directly into the involved artery in 12 patients and suppressed spasm in 9; in 3 patients, nifedipine increased coronary sinus flow, which had been decreased by spasm in one of the branches of the left coronary artery. Patients with Prinzmetal's variant angina who have spasm superimposed on atherosclerotic lesions can benefit from coronary arterial bypass grafting combined with partial denervation of the heart. This combination yielded acceptable results (83.4 percent favorable outcome); recurrence of attacks occurred in only 6.7 percent of this group. In those forms of angina in which spasm occurs in angiographically normal coronary arteries, therapy is essentially medical. In 13 patients treated with oral nifedipine (30 to 40 mg/day), suppression of attacks was achieved in 11 instances. During the period of treatment, the methergine provocative test, which had been consistently positive before treatment, converted to negative in 12 patients. Transient withdrawal of nifedipine caused recurrence of pain in two patients.