Vasospastic angina

ESC CardioMed ◽  
2018 ◽  
pp. 1427-1430
Author(s):  
Peter Ong ◽  
Udo Sechtem

The hallmark of vasospastic angina is angina at rest that promptly responds to short-acting nitrates. Classically, there is a preserved exercise capacity and the underlying mechanism is a focal occlusive spasm of the epicardial arteries with transient ST-segment elevation on the electrocardiogram (i.e. Prinzmetal’s, or variant angina). However, the clinical presentation of epicardial spasm may also comprise exercise-related symptoms. Intracoronary provocation testing with acetylcholine is the method of choice to establish the diagnosis and this can be performed with a good safety profile. Coronary spasm may occur in patients with normal or unobstructed coronary arteries but also in patients with epicardial stenoses and those with previous coronary revascularization. Distribution of epicardial spasm can be focal or diffuse and involve multiple locations. In European patients, diffuse spasm of the distal left anterior descending coronary artery is a frequent finding. Coronary spasm may also exist at the level of the coronary microcirculation which represents a form of coronary microvascular dysfunction. Despite good efficacy of calcium channel blockers and short-acting nitrates, a substantial number of patients have refractory symptoms. Apart from optimal risk factor control, emerging drugs for these patients include, for example, rho kinase inhibitors.

Author(s):  
Peter Ong ◽  
Udo Sechtem

Ischaemic heart disease comprises a variety of coronary abnormalities, ranging from obstructive atherosclerotic stenoses to functional coronary vasomotor disorders. The latter comprise coronary spasm, as well as coronary microvascular dysfunction. Importantly, structural and functional abnormalities can coexist in a given patient, making it sometimes difficult to determine the underlying cause of angina. Thus, diagnostic algorithms should not only consider the evaluation of atherosclerotic epicardial disease, but also look for the presence of functional coronary disorders. This holds especially true for patients in whom obstructive coronary disease has been excluded, as many of these patients are labelled as having ‘non-cardiac chest pain’. Such an approach may enable the treating physician to adjust the pharmacological therapy more appropriately, in order to improve symptoms and prognosis. Often drug classes such as calcium channel blockers and nitrates are beneficial in these patients. This chapter gives an overview on the current pharmacological management of patients with coronary artery spasm and those suffering from microvascular angina.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Probst ◽  
A Seitz ◽  
G Pirozzolo ◽  
A Becker ◽  
T Schaeufele ◽  
...  

Abstract Background Approximately 10% of patients with acute myocardial infarction do not have a culprit lesion. Such patients have been labelled as MINOCA (myocardial infarction with non-obstructive coronary arteries) and several pathophysiological etiologies have been described as potential explanations. This includes spontaneous coronary dissection, tako-tsubo-syndrome and coronary spasm. The latter can be diagnosed during invasive provocative testing. The aim of this study was to assess the frequency of coronary spasm and the safety of intracoronary provocation testing using acetylcholine in MINOCA patients compared to patients with stable angina and unobstructed coronary arteries. Methods Between 2007 and 2018 180 consecutive patients with either MINOCA or stable angina and unobstructed coronary arteries were enrolled. MINOCA was defined as acute onset of chest pain with either ST-segment elevation on the ECG or significant high sensitive troponin T elevation but no relevant epicardial stenosis (<50%) according to the current ESC guidelines. All patients underwent intracoronary acetylcholine provocation testing (ACH-test) in search of coronary spasm according to a standardized protocol immediately after diagnostic coronary angiography. Apart from systematic assessment of clinical, demographic and risk factor data, data regarding complications during the ACH-test were meticulously recorded. Results Eighty patients with MINOCA and 100 consecutive patients with stable angina were recruited (52% women, mean age 62±13 years). Overall, 59% had hypertension and 20% had diabetes. Comparison of clinical, demographic and risk factor data did not reveal any statistically significant differences except for a female preponderance in the stable patients (61% vs. 40%, p=0.007). The ACH-test revealed a coronary vasomotor disorder in 68% of cases. In 32% of cases the ACH-test was either inconclusive or negative. Epicardial spasm was found in 31% of patients with a higher prevalence among the MINOCA patients compared to the stable angina patients (41% vs. 23%, p=0.002). Microvascular spasm was found in 37% with a higher prevalence among the stable angina patients compared to the MINOCA cohort (49% vs. 23%, p=0.002). Assessment of complications during the ACH-test revealed that 13 MINOCA patients and 15 stable angina patients had minor complications such as intermittent atrioventricular block, sinusbradycardia, paroxysmal atrial fibrillation, ventricular ectopic beats or transient hypotension. Comparison of minor complications between the two groups did not reveal statistically significant differences (16% vs. 15%, p=0.839). None of the patients experienced any irreversible complications. Conclusion Coronary spasm is a frequent cause for MINOCA. Intracoronary spasm provocation testing using acetylcholine is feasible in such patients. The complication rate during ACH-testing in MINOCA patients is low and comparable to patients with stable angina. Acknowledgement/Funding Berthold-Leibinger-Foundation, Ditzingen, Germany


Author(s):  
Peter Ong ◽  
Udo Sechtem

Ischaemic heart disease comprises a variety of coronary abnormalities, ranging from obstructive atherosclerotic stenoses to functional coronary vasomotor disorders. The latter comprise coronary spasm, as well as coronary microvascular dysfunction. Importantly, structural and functional abnormalities can coexist in a given patient, making it sometimes difficult to determine the underlying cause of angina. Thus, diagnostic algorithms should not only consider the evaluation of atherosclerotic epicardial disease, but also look for the presence of functional coronary disorders. This holds especially true for patients in whom obstructive coronary disease has been excluded, as many of these patients are labelled as having ‘non-cardiac chest pain’. Such an approach may enable the treating physician to adjust the pharmacological therapy more appropriately, in order to improve symptoms and prognosis. Often drug classes such as calcium channel blockers and nitrates are beneficial in these patients. This chapter gives an overview on the current pharmacological management of patients with coronary artery spasm and those suffering from microvascular angina.


2020 ◽  
Vol 4 (3) ◽  
pp. 205-209
Author(s):  
Fabian Guenther ◽  
Andreas Seitz ◽  
Valeria Martínez Pereyra ◽  
Raffi Bekeredjian ◽  
Udo Sechtem ◽  
...  

A 43-year-old woman with recurrent atypical angina underwent invasive coronary angiography including intracoronary Doppler blood flow assessment and coronary spasm provocation testing. While obstructive epicardial disease could be ruled-out angiographically, the patient experienced reproduction of her angina symptoms after intracoronary administration of acetylcholine (100 µg) during spasm provocation testing. Simultaneously, the ECG showed new-onset ST-segment depression in the absence of epicardial spasm. In addition, coronary flow velocity was significantly reduced after acetylcholine compared to the baseline condition. Following intracoronary administration of nitroglycerine (200 µg), the patient’s symptoms as well as the ECG changes and coronary flow reduction were reversed. Considering the ongoing challenges in appropriate evaluation of the pathophysiological mechanisms of coronary microvascular dysfunction, simultaneous intracoronary Doppler flow measurement during spasm testing ‐ as shown in this case ‐ may provide objective evidence for microvascular spasm in addition to the standardized diagnostic criteria, especially if they are ambiguous.


2021 ◽  
Vol 22 (2) ◽  
pp. 484
Author(s):  
Martijn H. van der Ree ◽  
Jeroen Vendrik ◽  
Jan A. Kors ◽  
Ahmad S. Amin ◽  
Arthur A. M. Wilde ◽  
...  

Patients with Brugada syndrome (BrS) can show a leftward deviation of the frontal QRS-axis upon provocation with sodium channel blockers. The cause of this axis change is unclear. In this study, we aimed to determine (1) the prevalence of this left axis deviation and (2) to evaluate its cause, using the insights that could be derived from vectorcardiograms. Hence, from a large cohort of patients who underwent ajmaline provocation testing (n = 1430), we selected patients in whom a type-1 BrS-ECG was evoked (n = 345). Depolarization and repolarization parameters were analyzed for reconstructed vectorcardiograms and were compared between patients with and without a >30° leftward axis shift. We found (1) that the prevalence of a left axis deviation during provocation testing was 18% and (2) that this left axis deviation was not explained by terminal conduction slowing in the right ventricular outflow tract (4th QRS-loop quartile: +17 ± 14 ms versus +13 ± 15 ms, nonsignificant) but was associated with a more proximal conduction slowing (1st QRS-loop quartile: +12[8;18] ms versus +8[4;12] ms, p < 0.001 and 3rd QRS-loop quartile: +12 ± 10 ms versus +5 ± 7 ms, p < 0.001). There was no important heterogeneity of the action potential morphology (no difference in the ventricular gradient), but a left axis deviation did result in a discordant repolarization (spatial QRS-T angle: 122[59;147]° versus 44[25;91]°, p < 0.001). Thus, although the development of the type-1 BrS-ECG is characterized by a terminal conduction delay in the right ventricle, BrS-patients with a left axis deviation upon sodium channel blocker provocation have an additional proximal conduction slowing, which is associated with a subsequent discordant repolarization. Whether this has implications for risk stratification is still undetermined.


2020 ◽  
Author(s):  
Fan-xin Kong ◽  
Meng Li ◽  
Chun-Yan Ma ◽  
Ping-ping Meng ◽  
Yong-huai Wang ◽  
...  

Abstract Background Loeffler’s endocarditis is an inflammatory cardiac condition of hypereosinophilic syndrome which rarely involves coronary artery. When coronary artery is involved, known as eosinophilic coronary periarteritis, the clinical presentation, electrocardiographic changes and troponin level are extremely nonspecific and may mimic acute coronary syndrome. It is very important to make differential diagnosis for ECPA in order to avoid the unnecessary further invasive coronary angiography. Case presentation We report a case with chest pain, ST-segment depression in electrocardiogram and increased troponin-I mimicking acute non-ST-segment elevation myocardial infarction. However, quick echocardiography showed endomyocardial thickening with normal regional wall motion, which corresponded to the characteristics of Loeffler’s endocarditis. Emergent blood analysis showed marked increase in eosinophils and computed tomography angiography found no significant stenosis of coronary artery. Manifestations of magnetic resonance imaging consisted with findings of echocardiography. Finally, the patient was diagnosed as Loeffler’s endocarditis and possible coronary spasm secondary to eosinophilic coronary periarteritis. Conclusion This case exhibits the crucial use of quick transthoracic echocardiography and the emergent hematological examination for differential diagnosis in such scenarios as often if electrocardiogram change mimicking myocardial infarction.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Kensuke Nishimiya ◽  
Yasuharu Matsumoto ◽  
Jun Takahashi ◽  
Takeshi Kato ◽  
Kazuma Oyama ◽  
...  

Background: We have previously demonstrated that adventitial inflammation, including enhanced formation of adventitial vasa vasorum (VV), is involved in the pathogenesis of coronary spasm in porcine models and that optical frequency domain imaging (OFDI) allows us to visualize adventitial VV in humans in vivo. However, it remains to be elucidated whether adventitial VV is also involved in the coronary hyperconstriction in patients with vasospastic angina (VSA). In this study, we thus examined the extent of VV formation in VSA patients and control subjects by using OFDI. Methods: OFDI image acquisition of the left anterior descending coronary artery (LAD) was performed along the LAD at every 10 mm length after intracoronary administration of isosorbide dinitrate in 21 patients with acetylcholine-induced spasm and 10 control subjects without the spasm. Results: Patient characteristics were comparable between VSA patients and control subjects, including sex, age, cardiovascular risks and medications. OFDI and reconstructed 3D-OFDI images clearly visualized enhanced VV formation in VSA patients as compared with control subjects (Figure). Quantitative analysis showed that VV area was significantly larger in VSA patients than in control subjects (VSA, 0.093±0.006 vs. control, 0.040±0.006 mm 2 , P<0.0001), whereas vessel diameter, wall thickness and coronary lesion types were all comparable between the 2 groups. Conclusions: These results demonstrate for the first time that adventitial VV formation is enhanced at the spastic coronary segment in VSA patients, suggesting the important role of adventitial VV in the pathogenesis of coronary spasm.


2020 ◽  
Vol 16 (1) ◽  
pp. 43-49
Author(s):  
Sm Mustafa Zaman ◽  
Harisul Hoque ◽  
Khurshed Ahmed ◽  
Md Mukhlesur Rahman ◽  
Msi Tipu Chowdhury ◽  
...  

Structural and functional abnormalities of the microcirculation can impair myocardial perfusion which is called coronary microvascular dysfunction and the resulting ischemia is known as microvascular ischaemia. Most of the researches have focused on the epicardial coronary arteries while addressing angina pectoris. Although the importance of the coronary microcirculation in maintaining appropriate myocardial perfusion has been recognized for several decades, the substantial morbidity of coronary microvascular dysfunction (CMD) has not been appreciated until recently. It is not possible to diagnose of microvascular angina clinically with the current knowledge. Resting or exercise electrocardiogram is nondiagnostic. Imaging with speckle tracking in echocardiography may reveal focal diastolic and/or systolic dysfunction. Other noninvasive investigations includes, Contrast stress echocardiography, 99Tc-sestamibi imaging, cardiovascular magnetic resonance (CMR),Nuclear magnetic resonance spectroscopy may show some degree of abnormality. Invasive methods like intracoronary adenosine and acetylecholine test may guide us to diagnose CMD. No guideline directed medical therapy is still available for the CMD. Risk factors modification like smoking cessation and weight-loss may improve endothelial dysfunction and CMD. Beta blockers, calcium channel blockers, Angiotensin converting enzyme inhibitors and statin are now used in different clinical condition related to microvascular angina. After these medical treatment patient with microvascular angina have higher risk of MACE compared with people without angina. So, physicians must be aware of this potentially fatal but under recognized clinical entity. University Heart Journal Vol. 16, No. 1, Jan 2020; 43-49


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