Cardiovascular and Coronary Artery Imaging: Volume 2

Cardiovascular and Coronary Artery Imaging, Volume Two presents the basics of echocardiography, nuclear imaging and magnetic resonance imaging (MRI) and provides insights into their appropriate use. The book covers state-of-the-art approaches for automated non-invasive systems for early cardiovascular and coronary artery disease diagnosis. It includes several prominent imaging modalities such as MRI, CT and PET technologies. Other sections focus on major trends and challenges in this area and present the latest techniques for cardiovascular and coronary image analysis.

• Takes an integrated approach to cardiovascular and coronary imaging using machine learning, deep learning and reinforcement learning approaches
• Covers state-of-the-art approaches for automated non-invasive systems for early cardiovascular disease diagnosis
• Provides a perspective on future cardiovascular imaging and highlights areas that still need improvement

• Language: English
• Publisher: Academic Press
• Release date: Nov 22, 2022
• ISBN: 9780128227053

Book preview

Chapter 1

Predictors of outcome in ST-segment elevation myocardial infarction

Abou Bakr M. Salama¹, ², ³ and Ahmad Abdulsaboor⁴,    ¹Department of Cardiology, University of Louisville, Louisville, KY, United States,    ²Department of Cardiac Surgery, University of Verona, Verona, Italy,    ³Department of Cardiology, Zagazig University, Zagazig, Egypt,    ⁴Department of Clinical Pathology, Zagazig University, Zagazig, Egypt

Abstract

ST-segment elevation myocardial infarction (STEMI) caries high morbidity and mortality. Many clinical, lab as well as imaging criteria has been proposed to provide prognostic data after STEMI. Here, we spot the light on the most common predictors of outcome after STEMI.

Keywords

STEMI; prognosis after MI

Because most ST elevation myocardial infarction (STEMI) patients require reperfusion therapy, early risk assessment gives the patient and family an idea of what to expect in the future. Patients who are at an elevated risk of late arrhythmic or nonarrhythmic mortality are identified using late risk stratification. This process has two components: Early in-hospital identification of individuals at elevated risk of recurrent ischemia episodes, and identification of patients with an elevated risk of arrhythmic or nonarrhythmic death following a myocardial infarction (MI) [1].

First of all, the individual risk factors that influence prognosis in patients presented by STEMI that must be controlled properly to prevent recurrence of cardiac events.

The number of coronary heart disease (CHD) risk factors is very high. A family history of early CHD, as well as the four modifiable CHD risk factors (hypertension, smoking, dyslipidemia, and diabetes), predict the development of atherosclerosis and its clinical repercussions [2].

1.1 Clinical predictors

1.1.1 Heart failure

After cardiogenic shock, survival is still dismal. Despite vigorous reperfusion, cardiogenic shock and CHF are still the leading causes of death in STEMI patients having primary PCI. Future research should focus on interventions aimed at lowering mortality in these high-risk individuals [3].

The Killip classification divides individuals with an acute MI into two groups based on whether or not simple physical examination results imply LV dysfunction [4].

Class I: No evidence of heart failure (mortality 6%).

Class II: Findings of mild to moderate heart failure (S3 gallop, rales < halfway up lung fields or elevated jugular venous pressure) (mortality 17%).

Class III: Pulmonary edema (mortality 38%).

Class IV: Cardiogenic shock defined as systolic blood pressure <90 and signs of hypoperfusion such as oliguria, cyanosis, and sweating (mortality 67%).

The initial data from 1967 showed that each class had a higher mortality rate. This was before thrombolytic and/or PCI reperfusion treatment. The mortality rates in each class have decreased by 30%–50% due to breakthroughs in therapy.

1.1.2 Tachycardia

Patients with sustained heart rates more than 90 beats per minute had larger and more frequent anterior infarcts, severe LV dysfunction, and a dismal prognosis [5].

1.1.2.1 Electrocardiogram

The following ECG abnormalities, which usually suggest a bigger infarction, are associated with worse outcomes after STEMI. These include:

• Anterior compared to inferior infarcts.

• Higher number of leads showing ST elevation.

• Absence of ST elevation resolution for 90–180 minutes after fibrinolysis.

• Persistant ST elevation is rare except in the presence of ventricular aneurysm.

• Regardless of age, hypertension, diabetes, or renal function, the presence of a Q wave was a substantial predictor of death or hospitalization for ischemic heart disease (IHD) [6].

1.1.2.1.1 Ventricular arrhythmias

The development of ventricular tachycardia (VT) in the peri-MI period (i.e., within the first 48 hours after the MI) is thought to be attributable to temporary ischemia; nevertheless, the incidence of VT/VF and patient mortality rose as the patient’s baseline risk increased. Regardless of the underlying baseline risk, VT/VF remained an important predictive marker for the increased risk of clinical adverse events and 90-day mortality in STEMI patients following initial PCI [7].

1.1.2.2 Atrial fibrillation

A common consequence of acute myocardial infarction (AMI) is atrial fibrillation (AF), which is linked to increased morbidity and death in AMI patients [8].

1.1.2.3 Chronic kidney disease

The clinical characteristics of nondialysis-dependent advanced CKD patients with AMI are comparable to those of dialysis patients, and they are likely to have poor outcomes. Intensive efforts are needed to detect AMI in advanced CKD patients in a timely and accurate manner [9].

1.1.2.4 Peripheral artery disease

Intermittent claudication appears to be associated with poorer outcomes in STEMI patients. Men with intermittent claudication are at a higher risk of coronary artery disease than men who have had a heart attack [10].

Other factors might impact the outcome in patients who undergo PPCI including the time between the development of symptoms and PCI (also known as treatment delay), the time from arrival at the hospital to PCI (door-to-balloon time, or door-to-balloon delay), the length of time from initially contacting the healthcare system, presentation time (early vs late), the patient’s risk category, hospital and physician factors, and the significance of TIMI 3 flow (patent artery) [11].

1.1.3 Biomarkers

In patients with STEMI, a variety of biomarkers have been linked to risk. Troponin and CK-MB are the two most regularly used.

1.1.4 CK-MB

After myocardial damage, serum CK levels rise between 3–8 hours, peak within 12–24 hours, and recover to baseline within 3–4 days [12]. If the biomarker increases >20% above the level observed at the time of the recurring symptoms, both CK-MB and troponin can be utilized to diagnose episodes of reinfarction [13].

1.1.5 Troponin

Troponin I (cTnI) and T (cTnT) are regulatory proteins found in cardiac muscles that are sensitive and specific markers of myocardial necrosis. Elevated levels have prognostic significance; a value greater than the 99th percentile of the normal population should be considered an indication of MI [14].

1.1.6 High-sensitivity troponin assays

These high-sensitivity assays measure pg/mL levels of circulating troponin rather than ng/mL levels, allowing for not only increased sensitivity but also early diagnosis of myocardial necrosis. cTnI levels rose with time and were a reliable predictor of outcome [15].

1.1.7 Myoglobin

Myoglobin is a protein with a low molecular weight that is found in both cardiac and skeletal muscle. It can be found in the serum as soon as 2 hours after the onset of cardiac necrosis. Because myoglobin has a poor cardiac specificity but a high sensitivity, it can be used to rule out MI if the level is normal within the first 4–8 hours of symptoms [16].

1.2 Brain natriuretic peptide

High baseline BNP was linked to a number of negative clinical outcomes in STEMI patients undergoing primary PCI, including major bleeding, ischemic stroke, and cardiac death. After 3 years, higher BNP concentrations were no longer linked to MACE or all-cause mortality, but remained weakly linked to cardiac death [17].

It has been hypothesized that NT pro-BNP obtained within 24 hours of the onset of chest discomfort is more accurate in predicting mortality at 9 months than the TIMI risk score [18].

1.2.1 Ischemia-modified albumin

Ischemia-modified albumin is a sensitive ischemia marker that prevents albumin from binding to cobalt. Because IMA is a marker of ischemia rather than myocardial cell damage, little is known about its ability to predict long-term cardiac outcomes in patients with established acute myocardial infarction (AMI). However, IMA measured within 24 hours has recently been found to be a strong and independent predictor of cardiac outcome at one year in patients with AMI, which may help identify those who require more aggressive medical management [19].

1.2.2 Unbound free fatty acids

The association of serum unbound free fatty acid (FFAu) levels with mortality in patients presenting with STEMI in the Thrombolysis in Myocardial Infarction (TIMI) II trial found that FFAu was an independent risk factor for death as early as one day of hospitalization and continued to be an independent risk factor for death as late as one year after hospitalization [20].

1.2.3 Circulating microRNAs are new and sensitive biomarkers of myocardial infarction

The human transcriptome is divided into two types of RNA: coding and noncoding. Messenger RNAs (mRNAs) are coding RNAs that represent genes that will be translated into different proteins. Noncoding RNAs (ncRNAs) are a diverse category of molecules that cannot be translated into proteins. They include transfer RNAs (tRNAs), ribosomal RNAs (rRNAs), microRNAs (miRNAs), small nuclear RNAs (snRNAs), small nucleolar RNAs (snoRNAs), long noncoding RNAs (lncRNAs), and Piwi-interacting RNAs (piRNAs) [21,22].

MiRNAs are small regulatory noncoding RNAs with a length of roughly 22 nucleotides that affect the transcriptome [23]. The 21-nucleotide long lin-4 was the first miRNA to be described in the literature. It was first published in December 1993, when two distinct teams of researchers discovered it in the nematode C. elegans [24,25].

In patients with STEMI, higher levels of circulating miR-133a are linked to lower myocardial salvage, larger infarcts, and more severe reperfusion injury. In the setting of STEMI, miR-201a provides high diagnostic and prognostic value, as well as good predictive value for the occurrence of no-reflow [26,27].

1.2.4 Lipoprotein-associated phospholipase A2

In advanced atherosclerotic lesions, lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet-activating factor (PAF) acetyl hydrolase, is prevalent. The bulk and activity of plasma Lp-PLA2 acquired shortly after admission to the hospital for unstable angina or MI failed to predict death or recurrent major cardiovascular events. Another study found that measuring plasma Lp-PLA2 30 days after an acute coronary syndrome but not within 10 days predicts recurrent cardiovascular events [28].

1.2.5 Plasma fibrinogen level

According to one study, elevated plasma fibrinogen levels in STEMI patients following primary PCI are linked to ISR. Larger studies are needed to determine the predictive significance of fibrinogen in comparison to more difficult end-points [29].

1.2.6 Interleukin-6+, interleukin-10+, and interleukin-6-interleukin-10+ cytokine

Patients with STEMI can have very high circulating interleukin-6 (IL-6(+)) levels or very low circulating interleukin-6 (IL-6(−)) levels. IL10 was increased both in IL-6(+) STEMI and IL-6(−) STEMI patients, and IL-6(+) IL-10(+) STEMI patients had an increased risk of systolic dysfunction at discharge and death at 6 months. Researchers combined IL-10 and IL-6 in a formula that produced a risk score that exceeded any single cytokine in the prediction of systolic dysfunction and mortality [30].

1.2.7 Routinely feasible multiple biomarker score to predict prognosis after revascularized ST elevation myocardial infarction

After a revascularized acute MI, the long-term prognostic value of an easy-to-do multiple cardiac biomarker score was evaluated in order to evaluate a multimarker strategy to risk classification based on routine biomarkers.

It is possible to use BNP, hsCRP, creatininemia, and troponin I as part of a routine multimarker approach. The most powerful marker is BNP, and this multimarker method provides additional predictive information that aids in the identification of patients at high risk of clinical events [31].

1.2.8 Serum potassium

There is a link between serum potassium levels and in-hospital mortality in patients with acute MI. As a baseline, a blood potassium level of 3.5–4.0 mEq/L was used as a reference. It is worth noting that individuals with serum potassium levels between 4.5 and 5.0 mEq/L, previously thought to be within normal limits, had a roughly twofold higher risk of death than those with values between 3.5 and 4.0 mEq/L [32].

1.2.9 Glycemic control

In critically ill hyperglycemic patients admitted to an intensive care unit (ICU) with acute coronary syndrome, intensive blood glucose control with intravenous insulin infusion could minimize short-term and 30-day mortality, reinfarction stroke, and rehospitalization for congestive heart failure [33,34].

1.2.10 White blood cell count

In individuals with STEMI, an elevated white blood cell count on presentation has been linked to an increased risk of cardiac mortality. WBCs are a reliable predictor of infarct size as evaluated by cardiac magnetic resonance imaging 30 days following the initial percutaneous coronary intervention (PCI) [35].

1.3 Differential white blood cell count

Numerous research has looked into the relationship between thrombotic and inflammatory pathways in acute coronary syndromes. In acute STEMI, leukocytosis is a typical sign that indicates WBC infiltration into necrotic tissue in response to ischemia and reperfusion. The first leukocytes to be discovered in the injured cardiac region are neutrophils [36].

Neutrophils are the first leukocytes to be detected in the injured cardiac area and are eliminated from myocardial tissue after phagocytosing debris. Monocytes, on the other hand, migrate from capillaries to the extravascular space, where they become macrophages and exceed neutrophils 2–3 days after the acute episode. Macrophage-secreted cytokines increase monocytosis and boost fibroblast proliferation and collagen synthesis. Several studies have found that the number of leukocytes on a patient’s initial examination predicts their outcome in both short- and long-term follow-up [37–39].

Increased neutrophil count on admission to the hospital in individuals with AMI is linked to the onset of congestive heart failure [40]. After an AMI, peripheral monocytosis is linked to left ventricular dysfunction and the development of a left ventricular aneurysm. At various stages of the atherosclerotic process, lymphocytes play an important role in controlling the inflammatory response [41].

Lympopenia is a common observation following a stress reaction, second only to elevated corticosteroids, and has high discriminative ability for the diagnosis of acute myocardial infarction in this context [42,43]. A faulty clearance of apoptotic cells due to inadequate phagocytosis of apoptotic cells occurs in subsequent necrosis-inducing production of proinflammatory cytokines (tumor necrosis factor- and interlukin-6) under these pathologic settings. In addition, enhanced lymphocyte apoptosis has been linked to lymphopenia in critical inflammatory conditions [44].

In addition to being an independent measure of mortality, the neutrophil/lymphocyte ratio (N/L) exceeds the predictive information supplied by WBCs. In STEMI patients treated with early revascularization, N/L is a strong independent predictor of long-term mortality whether the link between N/L and long-term mortality is due to a fundamental pathophysiological process or is a marker of the severity of the ischemia episode