Prodromal Angina Research Articles

Potential Effects of Ischemic Postconditioning and Changes in Heat Shock Protein 72 in Patients with Acute Myocardial Infarction without Prodromal Angina.

The effectiveness of ischemic postconditioning (iPoC) in patients with ST-elevation myocardial infarction (STEMI) without ischemic preconditioning has not been determined. Therefore, we investigated the impact of iPoC and its potential mechanism related to heat shock protein 72 (HSP72) induction on myocardial salvage in patients with STEMI without prodromal angina (PA).We retrospectively analyzed data from 102 patients with STEMI with successful reperfusion among 323 consecutive patients with acute coronary syndrome. Among these, 55 patients with iPoC (iPoC (+) ) underwent 4 cycles of 60-second inflation and 30-second deflation of the angioplasty balloon. Both the iPoC (+) and iPoC (-) groups were divided into 2 further subgroups: patients with PA (PA (+) ) and those without (PA (-) ). We analyzed HSP72 levels in neutrophils, which were measured until 48 hours after reperfusion. I-123 β-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) scintigraphy was performed within a week of reperfusion therapy. In 64% of patients, thallium-201 (TL) scintigraphy was performed 6-8 months after STEMI onset.Using BMIPP and TL, in the PA (-) subgroups, the iPoC (+) group had a significantly greater myocardial salvage ratio than the iPoC (-) group. iPoC was identified as an independent predictor of the myocardial salvage ratio. The HSP72 increase ratio was significantly elevated in the iPoC (+) PA (-) group. Importantly, the myocardial salvage effect in patients without PA was significantly correlated with the HSP72 increase ratio, which was greater in patients with iPoC.These results suggest the potential impact of iPoC via HSP72 induction on myocardial salvage; however, the effects may be limited to patients with STEMI without PA.

THE FREQUENCY OF VSR (VENTRICULAR SEPTAL RUPTURE) AFTER ACUTE STEMI ST-ELEVATION MYOCARDIAL INFARCTION IN TERTIARY CARE HOSPITAL

The purpose of the study was to find out how frequently ventricular septal rupture occurred in patients who had an acute ST-elevation myocardial infarction and then visited the cardiology department of Lady Reading Hospital in Peshawar. The cross-sectional design was employed in the investigation, which took place between April 6, 2018, and April 12, 2018. A thorough history and standard physical examination were performed on 346 patients while under observation. Baseline tests such as transthoracic echocardiography and electrocardiography were carried out to evaluate ventricular septal rupture. Records included age, gender, type of STEMI, diabetes mellitus, smoking, history of CAD, and prodromal angina. The study's findings indicated that the patients' mean age was 53, with a standard deviation of ±11.23. Of the patients, 32% were female and 68% were male. Furthermore, ventricular septal rupture was present in 5% of the patients but not 95%. Thus, the study concludes that 5% of cases of ventricular septal rupture followed an acute ST-elevation myocardial infarction.

Clinical assessment of VSR site and size and its relation to the severity of heart failure in post-myocardial infarction ventricular septal rupture patients.

Ventricular septal rupture (VSR) is a rare but well-known mechanical consequence of an acute myocardial infarction (AMI). Even in the later stages of re-perfusion therapy, the result of VSR remains poor. Our aim is to assess the site and size of VSR in relation to the severity of cardiac failure. From January 2016 to December 2022, a total of 71 patients with a diagnosis of post-myocardial infarction VSR were admitted to the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Data records were retrospectively included in this registry. In all patients, clinical and echocardiographic data were gathered, and statistical analyses were performed. A total of 71 consecutive patients (mean age: 66.27 ± 8.88 years); 50.7% male, 49.3% female, with (M:F) ratio of almost (1:1). Left ventricular ejection fraction (LVEF) was (48.55 ± 10.44%) on echocardiography, and apical VSR was the most common site (69.0%). Overall, the VSD site was strongly related to the VSD size (p = .016), LVEF (p = .012), AMI site (p = .001), and affected coronary vessel (p = .004). Prodromal angina (p = .041), intra-aortic balloon pump (p = .002), affected coronary vessels (p = .020), pro-BNP (p = .000), and LVEF (p = .017) were predictors of the severity of heart failure. Diabetes mellitus is a common risk factor for post-myocardial infarction VSR. VSR site and size had no relation to the severity of heart failure. A presentation with prodromal angina predicted severe heart failure and a worse prognosis.

Ticagrelor Loading on ST-Elevation Myocardial Infarction: Interaction With Prodromal Angina on Infarct Size and Clinical Events.

Ticagrelor might reduce infarct size by exerting a more potent antiplatelet effect or by promoting a potential conditioning stimulus in ST-elevation myocardial infarction (STEMI) patients. Pre-infarction angina (PIA) is an effective preconditioning stimulus that reduces ischemia-reperfusion injury. Because little is known on the interaction of PIA in STEMI-patients loaded with ticagrelor, we sought to determine if patients loaded with ticagrelor had improved clinical outcomes as compared to clopidogrel and to study if it is modulated by the presence of PIA. From 1272 STEMI patients submitted to primary percutaneous coronary intervention and treated with clopidogrel or ticagrelor from January 2008 to December 2018, 826 were analyzed after propensity score matching. Infarct size was estimated using peak creatine kinase (CK) and troponin T (TnT), and clinical impact was evaluated through cumulative major cardiac and cerebrovascular events (MACCE) at 1-year follow-up. Matched patients and their interaction with PIA were analyzed. Patients loaded with ticagrelor had lower peak CK [1405.50 U/L (730.25-2491.00), P < .001] and TnT [3.58 ng/mL (1.73-6.59), P < .001)], regardless of PIA. The presence of PIA was associated with lower CK (P = .030), but not TnT (P = .097). There was no interaction between ticagrelor loading and PIA (P = .788 for TnT and P = .555 for CK). There was no difference in MACCE incidence between clopidogrel or ticagrelor loading (P = .129). Cumulative survival was also similar between clopidogrel or ticagrelor, regardless of PIA (P = .103). Ticagrelor reduced infarct sizes independently and without a synergic effect with PIA. Despite reducing infarct size, clinical outcomes were similar across both groups.

Relationship Between Prodromal Angina Pectoris and Neutrophil-to Lymphocyte Ratio in Patients With ST Elevation Myocardial Infarction

The aim of this study was to investigate the relationship between prodromal angina (PA) with neutrophil-to-lymphocyte ratio (NLR) in patients with ST-segment elevation myocardial infarction (STEMI). The study group included 145 patients with STEMI who underwent emergency coronary angiography (CA) within 24hours of symptom onset. Data were collected regarding whether patients had experienced PA before acute myocardial infarction. Seventy-three (73) patients (50.3%) had prodromal angina. Prodromal angina positive and negative groups were compared for demographic characteristics, complete blood count parameters including NLR, blood biochemistry parameters and left ventricular ejection fraction (LVEF). Neutrophil count, NLR, and troponin I levels were significantly higher in the PA negative group. LVEF after reperfusion and lymphocyte count were lower in the PA negative group. In multivariate regression analysis, NLR (β=-0.419, p<0.001) and LVEF (β=0.418, p<0.001) were found to be significantly associated with the presence of PA in STEMI patients. Absence of PA was significantly and independently associated with increased NLR and impaired LVEF after reperfusion, and increased NLR was found as a significant predictor for both lack of PA and impaired LVEF in STEMI patients.

Craniofacial Pain as the Sole Sign of Prodromal Angina and Acute Coronary Syndrome: A Review and Report of a Rare Case.

Orofacial pain can arise from different regions and etiologies. Some of the most debilitating pain conditions arise from the structures innervated by the trigeminal system (head, face, masticatory musculature, temporomandibular joint and associated structures). The problem with referred pain is the misdiagnosis and unnecessary therapy directed to the pain location instead of its origin. When craniofacial pain is the sole sign of myocardial ischemia, failure to recognize its cardiac source can endanger the patient. In particular, apart from unnecessary dental treatments, patients with acute myocardial infarction who do not experience chest pain run a very high risk of misdiagnosis and death. As endodontists, each of us may face many patients complaining of pain sensation in the teeth with the main source being other craniofacial/visceral organs. This review plots a diagnostically challenging case paving the way for further literature presentation in this regard. The aim of this compendious review was to gain knowledge about the prevalence, clinical characteristics and possible mechanisms of craniofacial pain of cardiac origin, in order to improve the clinician’s ability to make a correct diagnosis.

Prodromal angina is associated with myocardial salvage in acute ST-segment elevation myocardial infarction

Previous studies have shown that prodromal angina (PA) occurs frequently in acute myocardial infarction (MI) patients. However, the potential benefits of PA on ischaemic myocardial damage remain unknown. One-hundred and fifty-four patients with acute ST-segment elevation MI successfully treated with primary percutaneous coronary intervention (PPCI) were prospectively evaluated for new-onset PA in the week preceding infarction and other factors known to influence myocardial salvage. Cardiovascular magnetic resonance was performed 8 ± 3 days after MI for the assessment of area-at-risk (AAR), MI size, myocardial haemorrhage (MH), microvascular obstruction (MO), and myocardial salvage index (MSI). Patients with PA (n = 60) compared with those without PA (n = 94) showed similar AAR but significantly smaller MI size leading to larger MSI (0.53 ± 0.27 vs. 0.32 ± 0.26, P < 0.001). Additionally, patients with PA had lower incidence of MH (18 vs. 33%) and MO (22 vs. 46%) than non-PA patients (both P < 0.05). At univariate analysis, higher MSI was associated with new-onset PA, lower myocardial oxygen consumption before PPCI, shorter time-to-PPCI, and higher post-procedural TIMI flow-grade. Neither collateral circulation nor medications administered before PPCI were associated to MSI. After correction for other covariates by multivariate analysis, new-onset PA remained significantly associated with MSI (β-value: 0.352, P < 0.001). In acute MI patients, new-onset PA is associated with higher MSI independent of others factors known to influence jeopardized myocardium, as well as with less microvascular damage.

Presentations of acute coronary syndrome related to coronary lesion morphologies as assessed by intravascular ultrasound and optical coherence tomography

BackgroundPathologically, the lesions responsible for acute coronary syndrome (ACS) are ruptures of vulnerable plaques (and occasionally fibrous-cap erosions or calcified nodules) with a superimposed thrombosis. We aimed to clarify the clinical presentations related to the morphologies of coronary lesions of ACS using intravascular ultrasound (IVUS) and optical coherence tomography (OCT). Methods and resultsSeventy-five culprit lesions of ACS patients were clearly assessed with IVUS and OCT. Patients were classified into two groups based on the presence or absence of a rupture of a culprit plaque as identified by OCT. Clinical characteristics and lesion morphologies were compared between the two groups. Waist circumference was significantly greater (p<0.02) and prevalence of the metabolic syndrome (MS) higher (p=0.0011) in the rupture group. The prevalence of prodromal angina was higher in patients without plaque ruptures (p<0.0001). Using multivariate analysis, the MS and prodromal angina were independent predictors of rupture of a culprit coronary plaque (odds ratio (OR): 27.30, p<0.003 and OR: 0.04, p=0.0004, respectively). Among the components of the MS, the prevalence of abdominal obesity was a significant independent predictor of rupture of a culprit plaque (OR: 4.24, p<0.02). ConclusionsThere are two presentations related to the coronary lesion morphologies of ACS: we should understand these aspects of ACS.

Ischemic Preconditioning Effect of Prodromal Angina Is Attenuated in Acute Myocardial Infarction Patients With Hypertensive Left Ventricular Hypertrophy

Several animal experiments on acute myocardial infarction (AMI) have shown that the cardioprotective effects of ischemic preconditioning are more significant in hypertensive subjects. However, because there are no clinical data on the impact of hypertension on ischemic preconditioning in patients with AMI, whether clinical ischemic preconditioning of prodromal angina was beneficial in AMI patients with hypertension was investigated in the present study. 125 patients with a first anterior AMI who had undergone successful reperfusion therapy were divided into 2 groups, with or without hypertension, and into 2 further subgroups based on the presence or absence of prodromal angina. Dual-isotope (thallium-201(TL)/Tc-99m pyrophosphate) single-photon emission computed tomography (SPECT) was performed within 1 week of reperfusion therapy. Left ventricular (LV) function and LV mass index (LVMI) were measured by left ventriculography and echocardiography, respectively. In patients without hypertension, prodromal angina resulted in significantly less myocardial damage on TL-SPECT, better LV ejection fraction and a greater myocardial blush grade compared to patients without prodromal angina. However, these cardioprotective effects of prodromal angina were significantly diminished in hypertensive patients. Importantly, the myocardial salvage effects of prodromal angina showed a significant negative correlation with LVMI, which was significantly greater in hypertensive patients. The cardioprotective effects of prodromal angina were attenuated in patients with hypertension. Hypertensive LV hypertrophy may crucially limit the effects of ischemic preconditioning in AMI.

Craniofacial pain of cardiac origin is associated with inferior wall ischemia.

To investigate possible associations between the presence of craniofacial pain of cardiac origin and the location of cardiac ischemia and conventional risk factors. A total of 326 consecutive patients with confirmed myocardial ischemia (192 males, 134 females, mean age 64 years) were studied. Demographic details, health history, factors, prodromal symptoms, electrocardiogram (ECG) findings, and pain characteristics during the ischemic episode were assessed. The location of the ischemia according to the ECG findings was categorized as anterior, inferior, or lateral. Univariate chi-square analyses and a multivariate logistic regression model were used for data analysis. Two age subgroups (< 65 and > 65) were established when controlling for covariates. Craniofacial pain of cardiac origin was significantly associated with an inferior localization of cardiac ischemia (P < .001) and was more frequently reported in diabetic patients (P = .014). Thirty-eight patients (12%) did not experience chest pain during the myocardial ischemia. Nine patients (3%) experienced a prodromal angina episode without chest pain. The occurrence of craniofacial pain during myocardial ischemia, with or without an acute myocardial infarction, was associated with ischemia within the inferior wall. This result suggests the involvement of the vagal afferent system in the mechanisms of craniofacial pain of cardiac origin.

Effect of Prodromal Angina Pectoris on the Infarct Progression in Patients With First ST-Elevation Acute Myocardial Infarction

Prodromal angina pectoris (AP) has a cardioprotective effect by the mechanism of ischemic preconditioning, and the QRS score on the admission electrocardiogram (ECG) reflects myocardial damage at presentation. This study was undertaken to investigate the effect of prodromal AP on infarct progression after the onset of acute myocardial infarction (AMI). The study group comprised 291 patients with a first ST-elevation AMI who underwent coronary angiography within 24 h of symptom onset. QRS score was calculated from the admission ECG. Patients were divided into 3 groups according to elapsed time from onset of AMI to angiography: early group (<2 h), intermediate group (2-6 h) and late group (6-24 h). Prodromal AP was defined as angina occurring 24 h before the onset of AMI. Patients with prodromal AP (n=101; 35%) had a significantly lower QRS score than those without (2.4+/-2.4 vs 3.2+/-3.0, P=0.02). In patients without prodromal AP, the QRS score linearly increased as elapsed time increased: 2.6+/-2.8, 3.0+/-3.0 and 5.5+/-2.9 in the early, intermediate and late groups, respectively. In patients with prodromal AP, the QRS score remained low until 6 h after onset and then increased: 2.0+/-1.8, 2.0+/-2.1, and 4.1+/-3.3, respectively. The findings suggested that prodromal AP might delay infarct progression during the early hours after the onset of AMI and extend the window of time for reperfusion therapy.

Preinfarction angina prior to first myocardial infarction does not influence long-term prognosis: a retrospective study with subgroup analysis in elderly and diabetic patients.

Although prodromal angina occurring shortly before an acute myocardial infarction (MI) has protective effects against in-hospital complications, this effect has not been well documented after initial hospitalization, especially in older or diabetic patients. We examined whether angina 1 week before a first MI provides protection in these patients. A total of 290 consecutive patients, 143 elderly (>64 years of age) and 147 adults (<65 years of age), 68 of whom were diabetic (23.4%) and 222 nondiabetic (76.6%), were examined to assess the effect of preceding angina on long-term prognosis (56 months) after initial hospitalization for a first MI. No significant differences were found in long-term complications after initial hospitalization in these adult and elderly patients according to whether or not they had prodromal angina (44.4% with angina vs 45.4% without in adults; 45.5% vs 58% in elderly, P < 0.2). Nor were differences found according to their diabetic status (61.5% with angina vs 72.7% without in diabetics; 37.3% vs 38.3% in nondiabetics; P = 0.4). The occurrence of angina 1 week before a first MI does not confer long-term protection against cardiovascular complications after initial hospitalization in adult or elderly patients, whether or not they have diabetes.

Important factors for salvaging myocardium in patients with acute myocardial infarction

This study was designed to evaluate the factors that affect myocardial salvage after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). One hundred and eighty-three patients with AMI who had undergone successful PCI were recruited for this study. Patients underwent (99m)Tc-pyrophosphate single photon emission computed tomography (SPECT) on the third day and (99m)Tc-MIBI SPECT on the sixth day after admission. In the 20 SPECT segments, the summed defect score (TDS) and extent score (ES) of AMI segments were determined and the percentage of the salvaged myocardium was calculated based on the TDS and ES. We performed multivariate analysis to evaluate factors that can affect myocardial salvage. Multivariate analysis was performed among the value of myocardial salvage rate and the 15 clinical variables. Administration of nicorandil (p=0.006), prodromal angina (p<0.001), and high TIMI grade (p<0.001) had significant positive correlation to myocardial salvage rate. Use of a distal protection device had a significant negative correlation with myocardial salvage rate (p=0.006). The presence of high TIMI grade before PCI and prodromal angina are very important for salvaging myocardium. Furthermore, administration of nicorandil is important in salvaging myocardium in patients with AMI.

Effect of Intravenous Nicorandil and Preexisting Angina Pectoris on Short- and Long-Term Outcomes in Patients With a First ST-Segment Elevation Acute Myocardial Infarction

Published reports have indicated that prodromal angina before acute myocardial infarction (AMI) is associated with better outcomes and that nicorandil has cardioprotective effects on ischemic hearts. We compared cardioprotective effects of intravenous nicorandil with preconditioning effects by prodromal angina in patients with AMI who underwent percutaneous coronary intervention (PCI). In total, 368 patients with first ST-elevation AMI who underwent PCI were randomly assigned to receive nicorandil 12 mg or a placebo intravenously just before PCI. Subjects were assigned to 1 of 4 groups: 52 patients with prodromal angina were given placebo, 129 patients without prodromal angina were given nicorandil, 56 patients with prodromal angina were given nicorandil, and 131 patients without prodromal angina were given placebo. Coronary microvascular impairment after PCI was prevented at similar frequencies in groups with prodromal angina and groups on nicorandil. Five-year rates for freedom from major cardiac events were similar across groups with prodromal angina given placebo, without prodromal angina given nicorandil, and with prodromal angina given nicorandil (92.3%, 93.8%, and 92.9%, respectively) but were significantly lower in the group without prodromal angina given placebo (80.2%, p = 0.0019, 0.044, and 0.042, respectively). In conclusion, intravenous administration of nicorandil before PCI exerts pharmacologic cardioprotective effects similar to ischemic preconditioning in patients with AMI.

Right bundle-branch block in anterior acute myocardial infarction in the coronary intervention era: Acute angiographic findings and prognosis

Background Previous studies in the prethrombolytic or thrombolytic era have reported that right bundle-branch block (RBBB) is associated with poor clinical outcome in patients with acute myocardial infarction (AMI). Methods and Results The purpose of this study was to examine the relations between RBBB and angiographic findings or clinical outcomes in patients with AMI in the coronary intervention era. A total of 430 patients with a first anterior AMI who underwent coronary angiography within 12 h after the onset were enrolled in this study. Seventy-one patients (17%) had RBBB documented during their hospital stay. RBBB was documented on admission in 35 patients. Patients with RBBB were older ( p < 0.01) and had prodromal angina less frequently ( p = 0.03) than those without. On the initial angiograms, patients with RBBB had an occluded left anterior descending artery ( p < 0.01) and multivessel disease ( p = 0.01) more frequently than those without. Thirty-day mortality rate was significantly higher in patients with RBBB than in those without (14.0% vs 1.9%, p < 0.01). Multiple logistic-regression analysis demonstrated that RBBB (odds ratio 5.89, p < 0.01) and multivessel disease (odds ratio 4.36, p = 0.01) were independent predictors of 30-day mortality. Conclusions Our data suggested that RBBB was still associated with poor clinical outcome in patients with anterior AMI even in the coronary intervention era.

In-Hospital Mortality and Early Preinfarction Angina: a Meta-Analysis of Published Studies

The occurrence of preinfarction angina (PA) reduces the extent of myocardial necrosis, increases the volume of viable myocardium, and improves left ventricular function. However, there is no agreement about the effect of PA on mortality. The objective of this study was to determine whether PA is associated with in-hospital mortality. A meta-analysis (fixed effects model) of all published reports evaluating in-hospital mortality in patients with acute myocardial infarction according to the presence or absence of PA was performed. PA was defined as the occurrence of angina in the 24 hours before onset of the infarction. We searched the Medline and Embase databases in June 2004 using <<preinfarction angina or prodromal angina and mortality>> as search terms. Six studies involving a total of 3497 patients were finally identified. Only one study reported that PA had a statistically significant beneficial effect on in-hospital mortality. However, combining the data showed that the presence of PA was associated with a significant decrease in the probability of in-hospital death (odds ratio=0.61; 95% CI: 0.48-0.78; P<.0001. We did not detect any significant heterogeneity between the studies (chi2=5.92; P=.31). The occurrence of preinfarction angina in the 24 hours before the onset of myocardial infarction was associated with a significant reduction in in-hospital mortality of 39%.

Comparison of the cardioprotective effect of prodromal angina pectoris and collateral circulation in patients with a first anterior wall acute myocardial infarction

To compare the cardioprotective effect of prodromal angina pectoris and collateral circulation, 245 patients with first anterior acute myocardial infarction who underwent coronary angioplasty within 12 hours of symptoms were studied. Prodromal angina pectoris and collateral circulation were independently associated with higher predischarge left ventricular ejection fraction (LVEF), and a combination of prodromal angina pectoris and collateral circulation afforded cumulative improvement in LVEF in patients without diabetes mellitus. In patients with diabetes mellitus, collateral circulation, but not prodromal angina pectoris, was associated with higher predischarge LVEF.

Impact of prodromal angina pectoris and white blood cell count on outcome of patients with acute myocardial infarction

Background Elevation of white blood cell (WBC) count at admission is associated with adverse outcome after acute myocardial infarction (AMI). Prodromal angina, by the mechanism of ischemic preconditioning, improves left ventricular (LV) function and survival after reperfusion therapy in patients with AMI. Recent experimental studies have reported that preconditioning has anti-inflammatory effect. Methods This study consisted of 598 patients with first anterior wall AMI who underwent coronary angiography within 12 h after symptom onset. WBC count was measured at the time of hospital admission. Prodromal angina was defined as angina occurring within 24 h before the onset of AMI. Serial measurements of LV ejection fraction (EF) were obtained before reperfusion therapy and before discharge in 421 patients (71%). Results High WBC count (>10.2×10 3/mm 3, n=297) was associated with higher 30-day mortality (8% vs. 4%, p=0.02) and lower predischarge LVEF (51±15% vs. 57±14%, p<0.001), although there was no significant difference in acute LVEF (47±10% vs. 49±11%, p=0.07). High WBC count was an independent predictor of 30-day mortality ( p=0.009) and predischarge LVEF ( p=0.002). Prodromal angina was associated with lower 30-day mortality (3% vs. 7%, p=0.02) and preserved predischarge LVEF (57±15% vs. 53±14%, p=0.006). Patients with prodromal angina had lower WBC count (10.0±3.3×10 3/mm 3 vs. 11.0±3.9×10 3/mm 3, p=0.001) and prodromal angina was an independent predictor of WBC count ( p<0.001). Conclusions Elevation of WBC count and lack of prodromal angina were associated with impaired LV function and mortality after reperfusion in patients with AMI. Prodromal angina might have contributed to favorable outcome after AMI through its anti-inflammatory effect.

Myocardial injury and its prevention in the perioperative setting

Myocardial injury and its prevention in the perioperative setting

Usefulness of prodromal unstable angina pectoris in predicting better survival and smaller infarct size in acute myocardial infarction (The InTIME-II Prodromal Symptoms Substudy)

Prodromal unstable angina on presentation is a significant predictor of smaller infarct size, reflected by smaller creatine kinase-MB and creatine kinase total measurements and lower 30-day, 6-month, and 5-year mortality. These findings suggest that prodromal unstable angina is an important physiologic marker that should be routinely collected for risk stratification.