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 Table of Contents  
Year : 2021  |  Volume : 18  |  Issue : 1  |  Page : 31-34

Acute ST-elevation myocardial infarction in a patient with polycystic kidney disease in Kano, Nigeria

Department of Medicine, Aminu Kano Teaching Hospital, Kano, Nigeria

Date of Submission11-Oct-2020
Date of Decision07-Nov-2021
Date of Acceptance07-Jun-2022
Date of Web Publication11-Aug-2022

Correspondence Address:
Kamilu Musa Karaye
Department of Medicine, Aminu Kano Teaching Hospital, PMB 3452, Kano
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njc.njc_37_20

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A 37-year-old male patient known to have polycystic kidney disease (PKD) for the past 5 years presented with a 2-day history of severe chest pain at rest that was confirmed as acute inferior myocardial infarction (MI). He was a known hypertensive for the past 5 years with a difficult-to-control blood pressure, but with preserved renal function. He had no family history of similar illness and has no personal history of diabetes mellitus, dyslipidemia, smoking, alcohol consumption, or recreational drugs use. Apart from elevated blood pressure of 150/100 mmHg, physical examination was unremarkable. He was found to have dyslipidemia with high-density lipoprotein cholesterol of 0.87 mmol/l and hypertriglyceridemia (2.7 mmol/l), but other serum lipid fractions and fasting plasma glucose were within normal limits. His echocardiogram showed normal sizes of all cardiac chambers with preserved left ventricular (LV) function, inferior wall hypokinesia, and Grade I LV diastolic dysfunction, and he had no aortic aneurysm. He was admitted for 5 days, treated conservatively, and discharged after resolution of symptoms, troponin, and raised ST segments. To the best of our knowledge, this is the first report from Nigeria illustrating the rare association between PKD and acute MI in the young.

Keywords: Myocardial infarction, polycystic kidney disease, young

How to cite this article:
Muhammad B L, Ishaq NA, Ringim SH, Hamza SM, Abubakar HY, Abdulrahman S, Ahmad S A, Bashir FM, Abdulsalam T, Muhammad A, Alfa I, Sani RN, Bashir M, Salele S I, Sani H A, Hussain A, Kana SA, Mijinyawa MS, Sani MU, Karaye KM. Acute ST-elevation myocardial infarction in a patient with polycystic kidney disease in Kano, Nigeria. Nig J Cardiol 2021;18:31-4

How to cite this URL:
Muhammad B L, Ishaq NA, Ringim SH, Hamza SM, Abubakar HY, Abdulrahman S, Ahmad S A, Bashir FM, Abdulsalam T, Muhammad A, Alfa I, Sani RN, Bashir M, Salele S I, Sani H A, Hussain A, Kana SA, Mijinyawa MS, Sani MU, Karaye KM. Acute ST-elevation myocardial infarction in a patient with polycystic kidney disease in Kano, Nigeria. Nig J Cardiol [serial online] 2021 [cited 2023 Jan 30];18:31-4. Available from: https://www.nigjcardiol.org/text.asp?2021/18/1/31/353684

  Introduction Top

Polycystic kidney disease (PKD) is a multisystem disorder characterized by multiple bilateral renal cyst formation, with or without cystic changes in other organs, such as liver, pancreas, and the arachnoid membrane. Although it can also present as an autosomal recessive disease, it more commonly presents as an autosomal dominant disease with variable expression, due to mutations in two different genes, namely polycystin 1 (PC1) and polycystin 2 (PC2).[1],[2] PKD has worldwide distribution and has no racial discrimination. Its prevalence is estimated at about 1:400–1:1000 persons of the general population.[1] The prevalence of end-stage renal disease (ESRD) due to PKD is less among African–Americans perhaps because of higher incidence of other causes of ESRD.

The annual incidence of PKD was reported to be 2.73 cases per annum, and a family history of PKD and hypertension was present in 56.1% and 82.9%, respectively, while ESRD was seen in 19.5% (56.1% of them received hemodialysis) in a prospective study by Arogundade et al.[3] However, Chijioke et al. found that ESRD as the most common mode of presentation of PKD was seen in about 32% followed by hypertension.[4]

Hypertension is a major clinical feature and a predictor of outcomes in PKD, and several factors contribute to its development. PC1 and PC2 are expressed in vascular smooth muscle and endothelium and are associated with enhanced vascular smooth muscle contractility and impaired endothelium-dependent vasorelaxation.[5] These suggest that disruption of polycystin function contributes to the development of the hypertension.[5]

Autosomal dominant PKD (ADPKD) patients are at increased risk of developing cardiac valvular abnormalities such as mitral valve prolapse, as reported by Timio et al.[6] Several reports of spontaneous coronary artery dissection have been described in PKD patients.[7] Coronary artery ectasia is reported in about 1%–5% of coronary angiographies of PKD patients.[8] Krüger et al. have documented angina, positive stress exercise test, and pacing-induced ischemia in patients with coronary artery ectasia in the absence of significant coronary obstruction.[9] Although myocardial infarction (MI) has been reported in 38.7% of patients with coronary ectasia in general, cardiac events in ADPKD are seemingly low.[3],[9] The most frequent etiology of MI in PKD patients is accelerated coronary atherosclerosis, accounting for more than half of the cases.[9]

  Case Report Top

A 37-year-old male patient presented with PKD with systemic hypertension since 2015 attending follow-up at the Nephrology Clinic of Aminu Kano Teaching Hospital. The diagnosis was confirmed using abdominal ultrasound scan when he first presented with right loin pain, nausea, and hypertension in 2015, at the age of 32 years [Figure 1]. Serial abdominal ultrasound scans showed multiple cysts in both the kidneys, without involvement of the liver or other organs. He had been defaulting follow-up and has been poorly compliant with his antihypertensive treatment (lisinopril 5 mg once daily and bendrofluazide 2.5 mg once daily).
Figure 1: Renal ultrasound scan during hospitalization with acute myocardial infarction. Renal ultrasound scans of both kidneys multiple cysts in both kidneys (arrows). Cysts were not seen on other abdominal organs

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He presented to our emergency unit with a 2-day history of worsening chest pain, described as central, nonradiating, and unprovoked, associated with diaphoresis, breathlessness, and palpitations. There was no associated history of nausea or vomiting, intermittent calf claudication, syncope, or neurological deficit. He had never experienced similar symptoms in the past.

He was not known to have diabetes and has no family history of cardiovascular disease or sudden death. He had never used tobacco, ethanol, or any recreational drug.

Examination revealed a young male who was anxious, in painful distress, waist: hip ratio of 0.92, body mass index of 25 kg/m2, no pedal edema, and had peripheral oxygen saturation of 97% on ambient air. His heart rate was 88 beats/minute (bpm), blood pressure was 150/100 mmHg, and he had normal jugular venous pressure and heart sounds. Examination of other systems was unremarkable.

His electrocardiogram (ECG) at presentation showed sinus rhythm, heart rate of 78 bpm, left atrial enlargement, left ventricular (LV) hypertrophy, significant ST-segment elevation, and pathological Q waves in inferior leads (II, III, and arteriovenous fistula [aVF]) with reciprocal ST-depression in leads I, aVL, V5, and V6 [Figure 2]a. Initial cardiac troponin I was 5.63 ng/ml (reference, 0–0.5 ng/ml). His echocardiogram showed left atrial dimension of 41 mm, LV end-diastolic dimension of 48 mm, relative wall thickness of 0.48, LV mass index of 121 g/m2, LV ejection fraction of 54%, and pulmonary artery systolic pressure of 14.7 mmHg. There was hypokinesia of the inferior wall and had Grade I LV diastolic dysfunction. All valves, pericardium, thoracic, and abdominal aortic images were normal. A diagnosis of acute inferior STEMI with background PKD and hypertension was made, following which he was admitted. His baseline serum urea (12.4 mmol), creatinine (75.0 μmol), sodium (139 mmol), and potassium (3.7 mmol) were all within normal limits. Other biochemical results were fasting plasma glucose (4.1 mmol), serum total cholesterol (5.1 mmol), low-density lipoprotein cholesterol (3.03 mmol), high-density lipoprotein cholesterol (0.87 mmol/l), and triglycerides (2.7 mmol).
Figure 2: (a) Electrocardiogram at presentation with acute myocardial infarction. 12-Lead Electrocardiogram at presentation showing sinus rhythm, pathological Q-waves, ST-segment elevation with inverted T-waves in leads II, III, and aVF, and reciprocal ST-segment depression with/without T-wave inversion in the lateral leads. (b) Electrocardiogram at a follow-up visit. 12-Lead electrocardiogram at a follow-up visit showing sinus rhythm and pathological Q-waves in leads II, III, and aVF. aVF: Arteriovenous fistula

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The patient was treated conservatively with the following drugs: aspirin 300 mg stat (chewed) then aspirin 75 mg once daily per oral (PO), clopidogrel 75 mg once daily PO, metoprolol succinate 50 mg once daily PO, losartan 25 mg once daily PO, rosuvastatin 40 mg once daily PO, enoxaparin 1 mg/kg 12 hourly subcutaneously, and morphine 5 mg twice daily PO. He was clinically stable and pain free on the 2nd day of admission. The patient's overall condition improved significantly, and his heart rate was 76 bpm and BP was 110/80 mmHg on the 5th day of admission. His cardiac troponin I dropped to 0.26 ng/ml and the ST-segments also normalized on the 5th day of admission.

He was then discharged on the 5th day of admission and is being closely followed up. He was appropriately educated on his conditions and treatments and counseled on post-MI rehabilitation and lifestyle modification. During a review again at 4 weeks postdischarge, he was found to be asymptomatic, and his echocardiogram showed preserved LV geometry and systolic function, without regional wall motion abnormality, but with grade II LV diastolic dysfunction [Figure 3]. Serial ECGs postdischarge show sinus rhythm, pathological Q-waves in leads II, III, and aVF, and resolution of the previously raised ST-segments and inverted T-waves [Figure 2]b. The patient had been booked for computed tomographic (CT) coronary angiography in our facility for risk stratification and further management, but he has not been able to afford it.
Figure 3: Echocardiogram at 4 weeks postdischarge. Echocardiogram at 4 weeks postdischarge showing preserved LV size and systolic function, but with reversed e' (5.7 mm): a' (7.1 mm) ratio, suggestive of Grade II left ventricular diastolic dysfunction with high LV filling pressure. LV: Left ventricular

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  Discussion Top

In this report, we have described the case of acute inferior STEMI in a young male with known PKD and systemic hypertension, which to the best of our knowledge is the first report of such a case from Nigeria.

Even though MI is rare in patients with PKD, the possible causes of MI in the index case would include coronary artery dissection, coronary artery ectasia, and accelerated premature atherosclerosis that have been reported to occur in patients with PKD.[6],[7],[8] MI was reported in about 38.7% of patients with PKD due to coronary artery ectasia, but the most frequent etiology is coronary atherosclerosis, which occurs prematurely in patients with PKD.[3],[9]

Our patient had hypertension with poor blood pressure control due to poor adherence to treatment, which is associated with poor outcomes.[4],[10] However, he did not have other cardiovascular manifestations of PKD such as valvular abnormalities or aortic dissection.[7],[8] Thoracic aortic dissection is seven times more common in PKD than in the general population in autopsy series.[2] Several reports of spontaneous coronary artery dissection have been reported in PKD.[7]

The patient presented to us 2 days after the onset of angina, which is too late for thrombolytic therapy but which the patient would have qualified for, had he presented within the allowed window period of 12 h after onset of angina.[11] Another initial treatment option would have been primary angioplasty, but our center lacks facilities for cardiac catheterization or coronary angioplasty at present.

The long-term management of our patient would involve maintaining him on guideline-directed medical therapy, and defining his coronary anatomy using coronary CT angiography, in keeping with the lessons of the recent trial International Study of Comparative Health Effectiveness with Medical and Invasive Approaches (ISCHEMIA).[11],[12] In this trial, most enrolled trial patients underwent coronary CT angiography to rule out left main coronary disease and nonobstructive coronary disease.[12] Patients then underwent randomization if protocol-indicated clinical, ischemia-based, and anatomical eligibility criteria (based on blinded CT angiography) had been met. The results showed that among patients with stable coronary disease and moderate or severe ischemia, an initial invasive strategy, as compared with an initial conservative strategy, did not reduce the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years.

In the management of this patient, we acknowledge as a limitation the lack of cardiac catheterization laboratory for invasive coronary angiography and angioplasty, which is an option for managing the patient.

  Conclusion Top

We have reported the case of a young male with PKD and systemic hypertension, who presented to us with acute inferior STEMI, who was successfully managed conservatively, and who is being followed up. To the best of our knowledge, this is the first of such a case reported from Nigeria.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Torres VE, Harris PC, Pirson Y. Autosomal dominant polycystic kidney disease. Lancet 2007;369:1287-301.  Back to cited text no. 1
Torres VE, Harris PC. Autosomal dominant polycystic kidney disease: The last 3 years. Kidney Int 2009;76:149-68.  Back to cited text no. 2
Arogundade FA, Akinbodewa AA, Sanusi AA, Okunola O, Hassan MO, Akinsola A. Clinical presentation and outcome of autosomal dominant polycystic kidney disease in Nigeria. Afr Health Sci 2018;18:671-80.  Back to cited text no. 3
Chijioke A, Aderibigbe A, Olanrewaju TO, Makusidi AM, Oguntoyinbo AE, Braimoh KT. The prevalence and clinical characteristics of adult polycystic kidney disease in Ilorin, Nigeria. Port J Nephrol Hypert 2010;24:1-5.  Back to cited text no. 4
Qian Q, Hunter LW, Du H, Ren Q, Han Y, Sieck GC. Pkd2+/- vascular smooth muscles develop exaggerated vasocontraction in response to phenylephrine stimulation. J Am Soc Nephrol 2007;18:485-93.  Back to cited text no. 5
Timio M, Monarca C, Pede S, Gentili S, Verdura C, Lolli S. The spectrum of cardiovascular abnormalities in autosomal dominant polycystic kidney disease: A 10-year follow-up in a five-generation kindred. Clin Nephrol 1992;37:245-51.  Back to cited text no. 6
Lee CC, Fang CY, Huang CC, Ng SH, Yip HK, Ko SF. Computed tomography angiographic demonstration of an unexpected left main coronary artery dissection in a patient with polycystic kidney disease. J Thorac Imaging 2011;26:W4-6.  Back to cited text no. 7
Manginas A, Cokkinos DV. Coronary artery ectasias: Imaging, functional assessment and clinical implications. Eur Heart J 2006;27:1026-31.  Back to cited text no. 8
Krüger D, Stierle U, Herrmann G, Simon R, Sheikhzadeh A. Exercise-induced myocardial ischemia in isolated coronary artery ectasias and aneurysms (“dilated coronopathy”). J Am Coll Cardiol 1999;34:1461-70.  Back to cited text no. 9
Demopoulos VP, Olympios CD, Fakiolas CN, Pissimissis EG, Economides NM, Adamopoulou E, et al. The natural history of aneurysmal coronary artery disease. Heart 1997;78:136-41.  Back to cited text no. 10
Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The task force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39:119-77.  Back to cited text no. 11
Maron DJ, Hochman JS, Reynolds HR, Bangalore S, O'Brien SM, Boden WE, et al. Initial invasive or conservative strategy for stable coronary disease. N Engl J Med 2020;382:1395-407.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3]


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