Articles
<![CDATA[Anatomical and Hemodynamic Evaluation of Mitral Stenosis Patients with Echocardiography ]]>
<![CDATA[Muhammad Mukti]]>;
<![CDATA[Erwin Sukandi]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Syamsu Indra]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 5 No. 12 (2021): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
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DOI: 10.32539/bsm.v5i4.378
<![CDATA[Mitral stenosis (MS) is the most common valvular heart disease encountered in developing countries. The cause of MS is almost always chronic rheumatic heart disease. Echocardiography is the single most important diagnostic tool in the evaluation of MS. The objectives are to confirm the etiology, to assess the severity of stenosis, to recommend the type and timing of intervention, to assess other valvular lesions, presence of thrombus, and vegetation. According to current guidelines and recommendations for clinical practice, the severity of MS should not be defined by a single value but rather be assessed by a multimodality approach that determines valve areas, mean Doppler gradients, and pulmonary arterial pressures. The European Society of Echocardiography/American Society of Echocardiography (EAE/ASE) recommendations of measurement method for clinical practice were categorized into three level of recommendations. Mitral valve area (MVA) can be assessed by planimetry using either 2D or 3D imaging, pressure half-time (PTH), the continuity equation, and the proximal isovelocity surface area (PISA) method. These result echocardiographic examinations can increase the accuracy and appropriate management with a good prognosis.]]>
<![CDATA[Role of Fibroblast Growth Factor-23 in Coronary Slow Flow Phenomenon Pathogenesis ]]>
<![CDATA[Welly Oktaviandani]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Erwin Sukandi]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 5 No. 12 (2021): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
Show Abstract
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DOI: 10.32539/bsm.v5i4.379
<![CDATA[The phenomenon of angina chest pain without significant epicardial coronary artery stenosis, but accompanied by a slowdown in coronary blood flow is often found in patients with symptoms of acute coronary syndrome who undergoing invasive coronary angiography. This phenomenon of slow coronary blood flow is then called the coronary slow flow phenomenon (CSFP). The pathogenesis mechanism of CSFP remains unclear. The pathogenesis of CSFP is thought to be multifactorial. Endothelial dysfunction, small vessel disease, inflammation, renin system angiotensin aldosterone, atherosclerosis are thought to be involved in the pathogenesis of CSFP. Cardiovascular disease incidence and death were associated with elevated levels of Fibroblast growth factor-23 (FGF-23). High levels of FGF-23 can lead to formation of blood vessel calcification, left ventricular hypertrophy, arterial stiffness, endothelial dysfunction, increased inflammatory markers and elevated levels of angiotensin II. It is suspected that FGF-23 has a role in this event other than as a regulator of bone and mineral metabolism. This literature review aims to determine the relationship between fibroblast growth factor-23 and the pathophysiology of CSFP. Based on the broad role of FGF-23, it is possible that FGF-23 is involved in the pathogenesis of CSFP.]]>
<![CDATA[Coronary Microvascular Dysfunction ]]>
<![CDATA[Doharjo Manullang]]>;
<![CDATA[Imran Soleh]]>;
<![CDATA[Rukiah Chodilawati]]>;
<![CDATA[Syamsu Indra]]>;
<![CDATA[Ferry Usnizar]]>;
<![CDATA[Erwin Sukandi]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Ali Ghanie]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 5 No. 12 (2021): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
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DOI: 10.32539/bsm.v5i12.428
<![CDATA[Coronary microvascular dysfunction (DMK) is a condition of patients who are accompanied by complaints of chest pain where the results of coronary angiography examination are normal and this is almost 49% with 60% of patients diagnosed with DMK. Another study said that about 40% of patients with DMK showed coronary flow reserve (CFR <2) of about 40% and the WISE study (Women's Ischaemia Syndrome Evaluation) showed that about 47% of patients with chest pain had normal coronary arteries. DMK can be divided into 4 groups; DMK with no coronary arterial disease (CAD) obstruction and myocardial disease, DMK with myocardial disease where this occurs due to remodeling of intramural coronary arteries, DMK with CAD (coronary arterial disease) or acute myocardial infarction with or without ST segment, iatrogenic typhoid DMK occurs after coronary recanalization caused by vasoconstriction and distal embolization. The mechanism of action of DMK can be caused by several factors, namely endothelial dysfunction, smooth muscle dysfunction, decreased diastolic perfusion time, damage to blood vessels and damage to the vascular and microvascular remodeling. And to enforce this DMK, there are several tests carried out in diagnosing the disease, some of which are invasive and non-invasive so that by enforcing the diagnosis of this disease, treatment for DMK can be done immediately and optimally.]]>
<![CDATA[The Role of Percutaneous Ventricular Restoration Therapy in Heart Failure After Myocardial Infarction ]]>
<![CDATA[Yudhie Tanta]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Erwin Sukandi]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 6 No. 2 (2022): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
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DOI: 10.37275/bsm.v6i2.440
<![CDATA[The process of ventricular remodeling has a major role in the pathogenesis of heart failure in patients with myocardial infarction. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), antialdosterone diuretics, and beta receptor blockers are drugs that have been widely accepted as anti-remodeling agents. However, sometimes the efficacy of these drugs is inadequate, or their use is constrained by low blood pressure. Percutaneous ventricular restoration therapy is an action that aims to exclude segments of the myocardium that have akinetic or aneurysms by implanting a ventricular partitioning device percutaneously. This technique is expected to prevent the progression of ventricular remodeling through a procedure with a lower risk of intraprocedural mortality than the surgical approach.]]>
<![CDATA[Electrocardiography Predictive Value on Coronary Slow Flow Phenomenon ]]>
<![CDATA[Erwin Sukandi]]>;
<![CDATA[Yudhie Tanta]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Muhammad Irsan Saleh]]>;
<![CDATA[Irfannuddin]]>;
<![CDATA[Radiyati Umi Partan]]>;
<![CDATA[Zulkhair Ali]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 6 No. 3 (2022): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
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DOI: 10.37275/bsm.v6i3.454
<![CDATA[Coronary Slow Flow Phenomenon (CSFP) is characterized by the slow flow of contrast in one or more epicardial coronary vessels without evidence of coronary artery stenosis during coronary angiography procedures. CSFP is fairly common at the time of elective angiography with an incidence of around 7% and accounts for about 4% of hospitalized unstable angina cases. Coronary angiography is currently still the only effective way to detect CSFP, but this procedure is an invasive procedure with high costs, there is a risk of allergy to contrast. Electrocardiography (ECG), as a widely available, inexpensive, and simple modality is felt to be an attractive alternative in early detection of this abnormality. The ECG parameters on CSFP discussed in this study include; p-wave dispersion, QT interval dispersion, QRS intrinsic (Tpeak-Tenddeflection duration), and QRS fragmentation. Further studies are needed on the ECG image in CSFP so that in the future ECG can be a cheaper and non-invasive diagnostic modality for CSFP compared to coronary angiography.]]>
<![CDATA[Anatomical and Hemodynamic Evaluation of Mitral Stenosis Patients with Echocardiography ]]>
<![CDATA[Muhammad Mukti]]>;
<![CDATA[Erwin Sukandi]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Syamsu Indra]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 5 No. 12 (2021): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
Show Abstract
|
Download Original
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Original Source
|
Check in Google Scholar
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DOI: 10.32539/bsm.v5i4.378
<![CDATA[Mitral stenosis (MS) is the most common valvular heart disease encountered in developing countries. The cause of MS is almost always chronic rheumatic heart disease. Echocardiography is the single most important diagnostic tool in the evaluation of MS. The objectives are to confirm the etiology, to assess the severity of stenosis, to recommend the type and timing of intervention, to assess other valvular lesions, presence of thrombus, and vegetation. According to current guidelines and recommendations for clinical practice, the severity of MS should not be defined by a single value but rather be assessed by a multimodality approach that determines valve areas, mean Doppler gradients, and pulmonary arterial pressures. The European Society of Echocardiography/American Society of Echocardiography (EAE/ASE) recommendations of measurement method for clinical practice were categorized into three level of recommendations. Mitral valve area (MVA) can be assessed by planimetry using either 2D or 3D imaging, pressure half-time (PTH), the continuity equation, and the proximal isovelocity surface area (PISA) method. These result echocardiographic examinations can increase the accuracy and appropriate management with a good prognosis.]]>
<![CDATA[Role of Fibroblast Growth Factor-23 in Coronary Slow Flow Phenomenon Pathogenesis ]]>
<![CDATA[Welly Oktaviandani]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Erwin Sukandi]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 5 No. 12 (2021): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
Show Abstract
|
Download Original
|
Original Source
|
Check in Google Scholar
|
DOI: 10.32539/bsm.v5i4.379
<![CDATA[The phenomenon of angina chest pain without significant epicardial coronary artery stenosis, but accompanied by a slowdown in coronary blood flow is often found in patients with symptoms of acute coronary syndrome who undergoing invasive coronary angiography. This phenomenon of slow coronary blood flow is then called the coronary slow flow phenomenon (CSFP). The pathogenesis mechanism of CSFP remains unclear. The pathogenesis of CSFP is thought to be multifactorial. Endothelial dysfunction, small vessel disease, inflammation, renin system angiotensin aldosterone, atherosclerosis are thought to be involved in the pathogenesis of CSFP. Cardiovascular disease incidence and death were associated with elevated levels of Fibroblast growth factor-23 (FGF-23). High levels of FGF-23 can lead to formation of blood vessel calcification, left ventricular hypertrophy, arterial stiffness, endothelial dysfunction, increased inflammatory markers and elevated levels of angiotensin II. It is suspected that FGF-23 has a role in this event other than as a regulator of bone and mineral metabolism. This literature review aims to determine the relationship between fibroblast growth factor-23 and the pathophysiology of CSFP. Based on the broad role of FGF-23, it is possible that FGF-23 is involved in the pathogenesis of CSFP.]]>
<![CDATA[Coronary Microvascular Dysfunction ]]>
<![CDATA[Doharjo Manullang]]>;
<![CDATA[Imran Soleh]]>;
<![CDATA[Rukiah Chodilawati]]>;
<![CDATA[Syamsu Indra]]>;
<![CDATA[Ferry Usnizar]]>;
<![CDATA[Erwin Sukandi]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Ali Ghanie]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 5 No. 12 (2021): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
Show Abstract
|
Download Original
|
Original Source
|
Check in Google Scholar
|
DOI: 10.32539/bsm.v5i12.428
<![CDATA[Coronary microvascular dysfunction (DMK) is a condition of patients who are accompanied by complaints of chest pain where the results of coronary angiography examination are normal and this is almost 49% with 60% of patients diagnosed with DMK. Another study said that about 40% of patients with DMK showed coronary flow reserve (CFR <2) of about 40% and the WISE study (Women's Ischaemia Syndrome Evaluation) showed that about 47% of patients with chest pain had normal coronary arteries. DMK can be divided into 4 groups; DMK with no coronary arterial disease (CAD) obstruction and myocardial disease, DMK with myocardial disease where this occurs due to remodeling of intramural coronary arteries, DMK with CAD (coronary arterial disease) or acute myocardial infarction with or without ST segment, iatrogenic typhoid DMK occurs after coronary recanalization caused by vasoconstriction and distal embolization. The mechanism of action of DMK can be caused by several factors, namely endothelial dysfunction, smooth muscle dysfunction, decreased diastolic perfusion time, damage to blood vessels and damage to the vascular and microvascular remodeling. And to enforce this DMK, there are several tests carried out in diagnosing the disease, some of which are invasive and non-invasive so that by enforcing the diagnosis of this disease, treatment for DMK can be done immediately and optimally.]]>
<![CDATA[The Role of Percutaneous Ventricular Restoration Therapy in Heart Failure After Myocardial Infarction ]]>
<![CDATA[Yudhie Tanta]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Erwin Sukandi]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 6 No. 2 (2022): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
Show Abstract
|
Download Original
|
Original Source
|
Check in Google Scholar
|
DOI: 10.37275/bsm.v6i2.440
<![CDATA[The process of ventricular remodeling has a major role in the pathogenesis of heart failure in patients with myocardial infarction. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), antialdosterone diuretics, and beta receptor blockers are drugs that have been widely accepted as anti-remodeling agents. However, sometimes the efficacy of these drugs is inadequate, or their use is constrained by low blood pressure. Percutaneous ventricular restoration therapy is an action that aims to exclude segments of the myocardium that have akinetic or aneurysms by implanting a ventricular partitioning device percutaneously. This technique is expected to prevent the progression of ventricular remodeling through a procedure with a lower risk of intraprocedural mortality than the surgical approach.]]>
<![CDATA[Electrocardiography Predictive Value on Coronary Slow Flow Phenomenon ]]>
<![CDATA[Erwin Sukandi]]>;
<![CDATA[Yudhie Tanta]]>;
<![CDATA[Taufik Indrajaya]]>;
<![CDATA[Ali Ghanie]]>;
<![CDATA[Muhammad Irsan Saleh]]>;
<![CDATA[Irfannuddin]]>;
<![CDATA[Radiyati Umi Partan]]>;
<![CDATA[Zulkhair Ali]]>
<![CDATA[ Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 6 No. 3 (2022): Bioscientia Medicina: Journal of Biomedicine & Translational Research ]]>
Publisher : <![CDATA[HM Publisher ]]>
Show Abstract
|
Download Original
|
Original Source
|
Check in Google Scholar
|
DOI: 10.37275/bsm.v6i3.454
<![CDATA[Coronary Slow Flow Phenomenon (CSFP) is characterized by the slow flow of contrast in one or more epicardial coronary vessels without evidence of coronary artery stenosis during coronary angiography procedures. CSFP is fairly common at the time of elective angiography with an incidence of around 7% and accounts for about 4% of hospitalized unstable angina cases. Coronary angiography is currently still the only effective way to detect CSFP, but this procedure is an invasive procedure with high costs, there is a risk of allergy to contrast. Electrocardiography (ECG), as a widely available, inexpensive, and simple modality is felt to be an attractive alternative in early detection of this abnormality. The ECG parameters on CSFP discussed in this study include; p-wave dispersion, QT interval dispersion, QRS intrinsic (Tpeak-Tenddeflection duration), and QRS fragmentation. Further studies are needed on the ECG image in CSFP so that in the future ECG can be a cheaper and non-invasive diagnostic modality for CSFP compared to coronary angiography.]]>
