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[email protected] Current Pharmaceutical Design, 2017, 23, 1-6
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REVIEW ARTICLE
Advanced Strategies in the Diagnosis and Treatment of Patients with Coronary Artery Disease and Heart Failure: When Heart Failure Causes Ischemia and Angiotensin Converting Enzyme Inhibitor and Betablockers Helps in Diuresis Thach Nguyen1, Nguyen Van Lanh2, Vo Minh Viet2, Lam Hoang Phuc2, Trung N. Pham1, Khanh Duong3, Luke Ashwin Lawrence4, Vien T. Truong5 and Gianluca Rigatelli6 1
Department of Cardiovascular Research, Methodist Hospital, Merrillville IN; 2Tan Tao University, School of Medicine, Long An, Vietnam; 3Hue Central Hospital, Hue Vietnam; 4Escuela Latinoamerica de Medicina, Habana, Cuba; 5Pham Ngoc Thach University, School of Medicine, HCM city, Vietnam; 6Rovigo Hospital, Rovigo, Italy Abstract: In the diagnosis and management of patients with coronary artery disease (CAD) and chronic left ventricular (LV) dysfunction or heart failure (HF), there are many uncertainties because of the non-specificity of the symptoms and signs of HF. Usually, severe CAD causes LV dysfunction. However, not rarely, LV dysfunction is the cause or aggravation of ischemia to many subsets of patients with or without CAD. ARTICLE HISTORY Received: November 24, 2017 Accepted: December 20, 2017 DOI: 10.2174/1381612824666171227213456
In this article, the care of patients with CAD with LV dysfunction, along with the challenges of diagnosing asymptomatic HF and the criteria for monitoring success are presented. Then the evidence of LV dysfunction triggering or aggravating ischemia is discussed. The newest methodology of assessing the venous blood volume which causes the main presentations of HF when its filling capacity is exceeded will also be presented in details. In summary, the effects of fluid mobilization by conventional medications for CAD (e.g angiotensin converting enzyme inhibitors (ACEI) or beta-blockers (BB) and their therapeutic mechanisms are discussed. The goal of this review is to present the cardiologist consultants strong scientific evidence of detrimental interaction between CAD and LV dysfunction and the therapeutic action of ACEI and BB in the mobilization of venous fluid. As a result, the management of patients with CAD and HF could be exercised on an advanced level of expertise.
Keywords: Heart failure, Size and expansion of common femoral vein, Fluid overload, Venous fluid volume, Intravascular fluid volume. 1. INTRODUCTION In the diagnosis of patients with coronary artery disease (CAD) and chronic left ventricular (LV) dysfunction or heart failure (HF), there are many uncertainties because of the non-specificity of the symptoms and signs of HF. Once the patient improves, it is not clear what are the criteria for determination of success in the short and long-term management of acute or chronic HF, or for prevention of recurrences and re-admissions. In many situations, severe CAD causes LV dysfunction. However, not rarely, LV dysfunction was thought to be the cause or the aggravation of ischemia to many subsets of patients anywhere from no CAD to severe CAD [1]. In this article, we first review the care of patients with CAD with LV dysfunction, along with the challenges of diagnosing asymptomatic HF and the criteria for monitoring success. Then a short discussion about LV dysfunction triggering or aggravating ischemia is presented. Next, we suggest the newest methodology of assessing the venous blood volume which causes the main presentations of HF when its filling capacity is exceeded. In summary, the effects of fluid mobilization by conventional medications for CAD (e.g angiotensin converting enzyme inhibitors (ACEI) or betablockers (BB) and their therapeutic mechanisms are discussed. The goal of this review is to present the cardiologist consultants strong scientific evidence of detrimental interaction between CAD and LV dysfunction and the therapeutic action of ACEI and BB in the mobilization of venous fluid. As a result, the management of patients with CAD and HF could be exercised on an advanced level *Address correspondence to this author at the 200 E 86th Place, Merrillville IN 46410 USA; Tel: 219-756-1400; Fax: 219—756-1410; E-mail:
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of expertise which will benefit both the patients and the society that the cardiologist consultants serve. 2. FIRST PROBLEM 2.1. Non-specificity of the Symptoms and Signs of Heart Failure In the history interview and physical examination of patients with HF, their subjective complaints and objective physical findings are very non-specific. [2] The symptoms of shortness of breath (SOB), pitting edema in the extremities, the sound of crackles in the lungs upon auscultation, and the appearance of the jugular venous reflux, could be seen in many other medical conditions, such as severe chronic pulmonary embolism, pulmonary hypertension, and chronic obstructive pulmonary disease (COPD), etc. In the common strategy for investigation of HF, one of the main goals of physical examination is to assess the fluid level in every area of the body and to detect any fluid overload at its earliest stage. The usual areas of examination are listed in Table 1. However, the physical search for fluid overload could be negative because in well compensated patients or in very thin patients, there is only minimal or no edema. As the current investigative strategy is limited to the assessment of fluid level in the cardiovascular system or in other storage areas (abdominal wall, peritoneal cavity, scrotal area, presacral area, subcutaneous layer of the skin, etc), this search of fluid overload is believed to be too late of a reactive tactic and hardly represents an early pro-active strategy. The reason is that recurrent and refractory edema is a sign of advanced stage in HF. This is why there is a need for a non-invasive test which can detect at the earliest the almost
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Table 1. Areas of focus for physical examination in heart failure. 1.
Lower leg with edema at the ankle or at the shin
2.
Abdominal wall with fluid infiltration
3.
Dependent areas in the presacral area
4.
Liver congestion or hepatomegaly
5.
Extravascular fluid in the lungs with rales upon auscultation
6.
Jugular vein with distention or induced hepato-jugular reflux
7.
General outline of the face (puffy face) and the areas below the eyes
8.
The baggy skin in the arms, above the elbow
maximally filled level of the venous compartment. In that way, fluid overload rather than HF could be preemptively treated as once recurrent HF appears, it is too late for meaningful reversal.
Nguyen et al.
After correction of the low AOD and high LVEDP, the symptom of chest pain and EKG changes disappeared as the CPP reversed to the normal range (>30mmHg) (Fig. 2).
Fig. (2). Three months later at the office, the electrocardiogram of the same patient showed normal T waves in chest and limb leads. She had no more chest pain nor shortness of breath.
3. SECOND PROBLEM 3.1. Detrimental Interactions Between Coronary Artery Disease and Heart Failure In the care of patients with HF, many times, the cause of local or generalized hypokinesis of the wall of the left ventricle (LV) is CAD. However, the question was whether LV dysfunction or HF can cause chest pain and ischemia. [3] The rationale is that the coronary blood flow depends on the coronary perfusion pressure which is in turn controlled by the aortic diastolic pressure (AOD) and the LV end diastolic pressure (LVEDP). [4] The formula for perfusion of coronary arteries is calculated below.
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3.2. Coronary Perfusion Pressure (CPP) = AOD -LVEDP More blood is brought to the myocardium if the CPP is high, secondary to higher AOD or lower LVEDP or both. On the contrary, when the CPP is low and reaches a threshold (
